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Motosugi S, Takahashi N, Mineo S, Sato K, Tsuzuno T, Aoki-Nonaka Y, Nakajima N, Takahashi K, Sato H, Miyazawa H, Taniguchi K, Terai S, Tabeta K. Enrichment of Porphyromonas gingivalis in colonic mucosa-associated microbiota and its enhanced adhesion to epithelium in colorectal carcinogenesis: Insights from in vivo and clinical studies. PLoS One 2025; 20:e0320383. [PMID: 40131980 PMCID: PMC11936212 DOI: 10.1371/journal.pone.0320383] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2024] [Accepted: 02/17/2025] [Indexed: 03/27/2025] Open
Abstract
OBJECTIVES The oral-gut axis is believed to play a role in the pathogenesis of colorectal cancer (CRC). Previous studies have demonstrated the transmission of oral microbiota to the gut, disrupting gut microbial balance and creating a protumorigenic microenvironment conducive to CRC progression. Fusobacterium nucleatum is a putative periodontal pathogen recognized as a specific bacterium that promotes CRC development. However, the possible involvement of other periodontal pathogens in CRC is poorly understood. This study aimed to explore the effects of ingested periodontal pathogens on experimental CRC in mice and elucidate the underlying mechanisms. METHODS In this study, experimental colitis-induced CRC mouse models were used. The mice were orally administered periodontal pathogens (Porphyromonas gingivalis and Prevotella intermedia) three times a week during the experimental period. The CRC severity between the P. gingivalis-treated and P. intermedia-treated groups was compared. Lumen-associated microbiota (LAM) and mucosa-associated microbiota (MAM) were analyzed in both mouse and human samples. In vitro studies were conducted using intestinal epithelial cells to explore the possible mechanisms by which the periodontal pathogens affect the CRC development. RESULTS The P. gingivalis-treated group exhibited significantly increased CRC severity compared to the other groups among azoxymethane/dextran sodium sulfate (AOM/DSS)-induced mouse models. The LAM and MAM exhibited distinct bacterial compositions, and P. gingivalis was enriched more in MAM than in LAM. In vitro adhesion assays revealed that P. gingivalis had higher adhesive capacity to intestinal epithelial cells than P. intermedia and indicated the possible involvement of gingipains in such a capacity. CONCLUSION P. gingivalis is enriched in MAM, and its subsequent adhesion to intestinal epithelial cells is potentially involved in the progression of CRC.
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Affiliation(s)
- Shunya Motosugi
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Naoki Takahashi
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Shuhei Mineo
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Keisuke Sato
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Takahiro Tsuzuno
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Yukari Aoki-Nonaka
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Nao Nakajima
- Division of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Kazuya Takahashi
- Division of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Hiroki Sato
- Division of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Haruna Miyazawa
- Clinical and Translational Research Center, Niigata University Medical and Dental Hospital, Niigata, Japan
| | - Koji Taniguchi
- Department of Pathology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan
| | - Shuji Terai
- Division of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
| | - Koichi Tabeta
- Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
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Chatziparasidis G, Kantar A, Rafailia Chatziparasidi M, Fouzas S, Bush A, Chang A. The potential effects of climate change on non-cystic fibrosis bronchiectasis in children. Paediatr Respir Rev 2024:S1526-0542(24)00078-2. [PMID: 39592275 DOI: 10.1016/j.prrv.2024.10.002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/07/2024] [Revised: 10/04/2024] [Accepted: 10/04/2024] [Indexed: 11/28/2024]
Abstract
Climate change may have devastating effects on the pathogenesis of non-cystic fibrosis bronchiectasis in children since it affects the biological cycle of the respiratory pathogens and alters the human respiratory defense mechanisms. Bronchiectasis in children has been identified as an emerging global epidemic that has attracted the attention of the medical community over recent years. Pediatric pulmonologists should be aware of the consequences of climate change on children with bronchiectasis and plan strategies to ameliorate these effects.
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Affiliation(s)
| | - Ahmad Kantar
- Paediatric Asthma and Cough Centre, Gruppo Ospedaliero San Donato, Bergamo, and University Vita Salute San Raffaele, Milano, Italy
| | | | - Sotirios Fouzas
- Pediatric Respiratory Unit, School of Medicine, University of Patras, Patras, Greece
| | - Andrew Bush
- Departments of Paediatrics and Paediatric Respiratory Medicine, Royal Brompton Harefield NHS Foundation Trust and Imperial College, London, UK
| | - Anne Chang
- Department of Respiratory and Sleep Medicine, Queensland Children's Hospital, Brisbane, Australia; Australian Centre for Health Services Innovation, Queensland University of Technology, Brisbane, Australia; Child Health Division, Menzies School of Health Research, Darwin, Australia
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Ma J, Chiu YF, Kao CC, Chuang CN, Chen CY, Lai CH, Kuo ML. Fine particulate matter manipulates immune response to exacerbate microbial pathogenesis in the respiratory tract. Eur Respir Rev 2024; 33:230259. [PMID: 39231594 PMCID: PMC11372469 DOI: 10.1183/16000617.0259-2023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2023] [Accepted: 06/18/2024] [Indexed: 09/06/2024] Open
Abstract
Particulate matter with a diameter ≤2.5 μm (PM2.5) poses a substantial global challenge, with a growing recognition of pathogens contributing to diseases associated with exposure to PM2.5 Recent studies have focused on PM2.5, which impairs the immune cells in response to microbial infections and potentially contributes to the development of severe diseases in the respiratory tract. Accordingly, changes in the respiratory immune function and microecology mediated by PM2.5 are important factors that enhance the risk of microbial pathogenesis. These factors have garnered significant interest. In this review, we summarise recent studies on the potential mechanisms involved in PM2.5-mediated immune system disruption and exacerbation of microbial pathogenesis in the respiratory tract. We also discuss crucial areas for future research to address the gaps in our understanding and develop effective strategies to combat the adverse health effects of PM2.5.
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Affiliation(s)
- Jason Ma
- Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan
- Equal contribution to this work
| | - Ya-Fang Chiu
- Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan
- Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan
- Research Center for Emerging Viral Infections, Chang Gung University, Taoyuan, Taiwan
- Department of Laboratory Medicine, Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Linkou, Taiwan
- Division of Infectious Diseases, Department of Medicine, Chang Gung Memorial Hospital, New Taipei, Taiwan
- Equal contribution to this work
| | - Chih-Chen Kao
- School of Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan
| | - Chun-Ning Chuang
- Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan
| | - Chi-Yuan Chen
- Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan
| | - Chih-Ho Lai
- Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan
- Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan
- Research Center for Emerging Viral Infections, Chang Gung University, Taoyuan, Taiwan
- Department of Laboratory Medicine, Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Linkou, Taiwan
- Department of Microbiology and Immunology, School of Medicine, China Medical University, Taichung, Taiwan
- Department of Nursing, Asia University, Taichung, Taiwan
- Equal contribution to this work
| | - Ming-Ling Kuo
- Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan
- Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan
- Division of Allergy, Asthma, and Rheumatology, Department of Pediatrics, Chang Gung Memorial Hospital, Linkou, Taiwan
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Liu Q, Deng J, Yan W, Qin C, Du M, Wang Y, Zhang S, Liu M, Liu J. Burden and trends of infectious disease mortality attributed to air pollution, unsafe water, sanitation, and hygiene, and non-optimal temperature globally and in different socio-demographic index regions. Glob Health Res Policy 2024; 9:23. [PMID: 38937833 PMCID: PMC11212388 DOI: 10.1186/s41256-024-00366-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/21/2024] [Accepted: 06/20/2024] [Indexed: 06/29/2024] Open
Abstract
BACKGROUND Environmental factors greatly impact infectious disease-related mortality, yet there's a lack of comprehensive global studies on the contemporary burden and trends. This study aims to evaluate the global burden and trends of infectious disease mortality caused by air pollution, unsafe water, poor sanitation, and non-optimal temperature across Socio-Demographic Index (SDI) regions from 1990 to 2019. METHODS This observational study utilized data from the Global Burden of Diseases Study to examine mortality rates from infectious diseases attributed to environmental risk factors between 1990 and 2019, including air pollution, unsafe water, sanitation, handwashing facilities (UWSH), and non-optimal temperatures. Age-standardized mortality rates (ASMRs) and estimated annual percentage change (EAPC) were utilized to present infectious disease mortality, and its trajectory influenced by environmental risk factors over the years. Nonlinear regression was conducted to explore the association between the SDI and ASMRs across regions from 1990 to 2019. RESULTS In 2019, global infectious disease deaths linked to air pollution, UWSH, and non-optimal temperature reached a startling 2,556,992. Disease mortality varied widely across SDI regions, with the highest number of deaths due to air pollution and UWSH in Low SDI regions, and deaths from non-optimal temperature primarily in High SDI regions. Age disparities emerged, with children under five and the elderly most affected. However, an increasing mortality trend was observed among seniors (65-69, 75-79, and over 80) in High SDI regions due to enteric infections linked to UWSH. Globally, a consistent decrease in ASMR was seen from 1990 to 2019 for all diseases connected to these factors, except for respiratory infections linked to non-optimal temperature. CONCLUSIONS Our study underscores the significant impact of air pollution, UWSH, and non-optimal temperatures on global infectious disease mortality, particularly among vulnerable groups such as children and the elderly. It's important to tackle these challenges with targeted interventions aiming to enhance environmental quality, improve water and sanitation systems, and control extreme temperatures. In addition, international cooperation is essential for bridging regional disparities and driving global public health initiatives forward, thereby helping achieve Sustainable Development Goals more effectively.
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Affiliation(s)
- Qiao Liu
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Jie Deng
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Wenxin Yan
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Chenyuan Qin
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Min Du
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Yaping Wang
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Shimo Zhang
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
| | - Min Liu
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China
- Key Laboratory of Epidemiology of Major Diseases, Ministry of Education, Peking University, Haidian District, Beijing, China
| | - Jue Liu
- Department of Epidemiology and Biostatistics, School of Public Health, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, 100191, China.
- Key Laboratory of Epidemiology of Major Diseases, Ministry of Education, Peking University, Haidian District, Beijing, China.
- Institute for Global Health and Development, Peking University, Haidian District, Beijing, China.
- Global Center for Infectious Disease and Policy Research & Global Health and Infectious Diseases Group, Peking University, Beijing, China.
- Institute of Environmental Medicine, Peking University, Beijing, China.
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Ryu MH, Murphy S, Hinkley M, Carlsten C. COPD Exposed to Air Pollution: A Path to Understand and Protect a Susceptible Population. Chest 2024; 165:836-846. [PMID: 37972689 DOI: 10.1016/j.chest.2023.11.012] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/18/2023] [Revised: 09/14/2023] [Accepted: 11/09/2023] [Indexed: 11/19/2023] Open
Abstract
TOPIC IMPORTANCE Air pollution poses a risk to the respiratory health of individuals with COPD. Long- and short-term exposures to higher levels of particulate-rich air pollution are associated with increased COPD exacerbation, hospitalization, and mortality, collectively implicating air pollution as a cause of adverse COPD-related outcomes. REVIEW FINDINGS This review summarizes the evidence for COPD as a phenotype that confers susceptibility for adverse health outcomes in the face of common air pollution. We highlight how typical contributors to compromised urban air quality, including that from traffic, wildfire smoke, and indoor biomass combustion, adversely affect the COPD patient population. Evidence underscoring the burden of ongoing air pollution exposure on patients with COPD is discussed. We then detail the detrimental impact of that exposure on COPD pathophysiology, which in turn increases the patient's susceptibility. We specifically propose that indoor air is a particularly rational target for increased monitoring and remediation to protect patients with COPD. Because COPD is a heterogeneous disease with several endotypes, future intervention studies need to better include control populations, to highlight COPD-specific risks and identify subpopulations within patients with COPD who will benefit the most from improved indoor air quality. SUMMARY Regulatory efforts must continue to broadly lower emission standards to protect this susceptible population from the negative health impacts of air pollution.
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Affiliation(s)
- Min Hyung Ryu
- Air Pollution Exposure Laboratory, Division of Respiratory Medicine, The University of British Columbia, Vancouver, BC, Canada
| | - Shane Murphy
- Air Pollution Exposure Laboratory, Division of Respiratory Medicine, The University of British Columbia, Vancouver, BC, Canada
| | - Madison Hinkley
- Air Pollution Exposure Laboratory, Division of Respiratory Medicine, The University of British Columbia, Vancouver, BC, Canada
| | - Chris Carlsten
- Air Pollution Exposure Laboratory, Division of Respiratory Medicine, The University of British Columbia, Vancouver, BC, Canada; Legacy for Airway Health and Centre for Lung Health, Vancouver Coastal Health Research Institute, Vancouver, BC, Canada.
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6
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Olsson H, Tamire M, Samuelsson E, Addissie A, Andersson R, Skovbjerg S, Athlin S. Household air pollution and pneumococcal density related to nasopharyngeal inflammation in mothers and children in Ethiopia: A cross-sectional study. PLoS One 2024; 19:e0297085. [PMID: 38271409 PMCID: PMC10810524 DOI: 10.1371/journal.pone.0297085] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2023] [Accepted: 12/22/2023] [Indexed: 01/27/2024] Open
Abstract
BACKGROUND Three billion people in low- and middle-income countries are exposed to household air pollution as they use biomass fuel for cooking. We investigated the associations between solid fuel use and nasopharyngeal (NP) inflammation, as well as the associations between high pneumococcal density and NP inflammation, in mothers and children in rural and urban Ethiopia. MATERIALS AND METHODS Sixty pairs of mothers (median age, 30 years; range, 19-45 years) with a child (median age, 9 months; range, 1-24 months) were included from rural Butajira (n = 30) and urban Addis Ababa (n = 30) in Ethiopia. The cohort was randomly selected from a previous study of 545 mother/child pairs included 2016. Questionnaire-based data were collected which included fuel type used (solid: wood, charcoal, dung or crop waste; cleaner: electricity, liquefied petroleum gas). Nasopharyngeal (NP) samples were collected from all mothers and children and analyzed for the levels of 18 cytokines using a Luminex immunoassay. Pneumococcal DNA densities were measured by a real-time multiplex PCR and a high pneumococcal density was defined as a cyclic threshold (Ct) value ≤ 30. RESULTS Mothers from rural areas had higher median CXCL8 levels in NP secretions than those from urban areas (8000 versus 1900 pg/mL; p < 0.01), while rural children had slightly higher IL-10 levels than those from the urban area (26 vs 13 pg/mL; p = 0.04). No associations between fuel type and cytokine levels were found. However, a high pneumococcal density was associated with higher levels of cytokines in both mothers (CCL4, CXCL8, IL-1β, IL-6 and VEGF-A) and children (CCL4, CXCL8, IL-1β, IL-6 and IL-18). CONCLUSIONS No significant associations were found between solid fuel use and NP inflammation in Ethiopian mothers and children, but the inflammatory activity was higher in individuals living in the rural compared to the urban area. In addition, high cytokine levels were associated with high pneumococcal density in both mothers and children, indicating a significant impact of NP pathogens on inflammatory mediator levels in upper airways.
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Affiliation(s)
- Henrik Olsson
- Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden
| | - Mulugeta Tamire
- Department of Preventive Medicine, School of Public Health, Addis Ababa University, Addis Ababa, Ethiopia
| | - Ebba Samuelsson
- Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
- Department of Clinical Microbiology, Sahlgrenska University Hospital, Region Västra Götaland, Gothenburg, Sweden
| | - Adamu Addissie
- Department of Preventive Medicine, School of Public Health, Addis Ababa University, Addis Ababa, Ethiopia
| | - Rune Andersson
- Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
- Department of Clinical Microbiology, Sahlgrenska University Hospital, Region Västra Götaland, Gothenburg, Sweden
| | - Susann Skovbjerg
- Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
- Department of Clinical Microbiology, Sahlgrenska University Hospital, Region Västra Götaland, Gothenburg, Sweden
| | - Simon Athlin
- Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden
- School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden
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Inesta-Vaquera F, Miyashita L, Grigg J, Henderson CJ, Wolf CR. Defining the in vivo mechanism of air pollutant toxicity using murine stress response biomarkers. THE SCIENCE OF THE TOTAL ENVIRONMENT 2023; 888:164211. [PMID: 37196967 DOI: 10.1016/j.scitotenv.2023.164211] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/15/2022] [Revised: 05/10/2023] [Accepted: 05/12/2023] [Indexed: 05/19/2023]
Abstract
Air pollution can cause a wide range of serious human diseases. For the informed instigation of interventions which prevent these outcomes there is an urgent need to develop robust in vivo biomarkers which provide insights into mechanisms of toxicity and relate pollutants to specific adverse outcomes. We exemplify for a first time the application of in vivo stress response reporters in establishing mechanisms of air pollution toxicity and the application of this knowledge in epidemiological studies. We first demonstrated the utility of reporter mice to understand toxicity mechanisms of air pollutants using diesel exhaust particles compounds. We observed that nitro-PAHs induced Hmox1 and CYP1a1 reporters in a time- and dose-dependent, cell- and tissue-specific manner. Using in vivo genetic and pharmacological approaches we confirmed that the NRF2 pathway mediated this Hmox1-reporter induction stress reporter activity. We then correlated the activation of stress-reporter models (oxidative stress/inflammation, DNA damage and Ah receptor -AhR- activity) with responses in primary human nasal cells exposed to chemicals present in particulate matter (PM; PM2.5-SRM2975, PM10-SRM1648b) or fresh roadside PM10. To exemplify their use in clinical studies, Pneumococcal adhesion was assessed in exposed primary human nasal epithelial cells (HPNEpC). The combined use of HPNEpC and in vivo reporters demonstrated that London roadside PM10 particles induced pneumococcal infection in HPNEpC mediated by oxidative stress responses. The combined use of in vivo reporter models with human data thus provides a robust approach to define the relationship between air pollutant exposure and health risks. Moreover, these models can be used in epidemiological studies to hazard ranking environmental pollutants by considering the complexity of mechanisms of toxicity. These data will facilitate the relationship between toxic potential and the level of pollutant exposure in populations to be established and potentially extremely valuable tools for intervention studies for disease prevention.
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Affiliation(s)
- Francisco Inesta-Vaquera
- Division of Systems Medicine, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital, Dundee DD1 9SY, UK
| | | | | | - Colin J Henderson
- Division of Systems Medicine, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital, Dundee DD1 9SY, UK
| | - C Roland Wolf
- Division of Systems Medicine, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital, Dundee DD1 9SY, UK.
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8
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Chen Y, Wu Y, Qi Y, Liu S. Cell Death Pathways: The Variable Mechanisms Underlying Fine Particulate Matter-Induced Cytotoxicity. ACS NANOSCIENCE AU 2023; 3:130-139. [PMID: 37101591 PMCID: PMC10125306 DOI: 10.1021/acsnanoscienceau.2c00059] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/30/2022] [Revised: 01/10/2023] [Accepted: 01/10/2023] [Indexed: 04/28/2023]
Abstract
Recently, the advent of health risks due to the cytotoxicity of fine particulate matter (FPM) is concerning. Numerous studies have reported abundant data elucidating the FPM-induced cell death pathways. However, several challenges and knowledge gaps are still confronted nowadays. On one hand, the undefined components of FPM (such as heavy metals, polycyclic aromatic hydrocarbons, and pathogens) are all responsible for detrimental effects, thus rendering it difficult to delineate the specific roles of these copollutants. On the other hand, owing to the crosstalk and interplay among different cell death signaling pathways, precisely determining the threats and risks posed by FPM is difficult. Herein, we recapitulate the current knowledge gaps present in the recent studies regarding FPM-induced cell death, and propose future research directions for policy-making to prevent FPM-induced diseases and improve knowledge concerning the adverse outcome pathways and public health risks of FPM.
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Affiliation(s)
- Yucai Chen
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, Beijing 100085, China
- University
of Chinese Academy of Sciences, Beijing 100049, China
| | | | - Yu Qi
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, Beijing 100085, China
- University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Sijin Liu
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, Beijing 100085, China
- University
of Chinese Academy of Sciences, Beijing 100049, China
- Science
and Technology Innovation Center, Shandong
First Medical University & Shandong Academy of Medical Sciences, Jinan 250000, China
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9
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Li N, Zhou H, Holden VK, Deepak J, Dhilipkannah P, Todd NW, Stass SA, Jiang F. Streptococcus pneumoniae promotes lung cancer development and progression. iScience 2023; 26:105923. [PMID: 36685035 PMCID: PMC9852931 DOI: 10.1016/j.isci.2022.105923] [Citation(s) in RCA: 24] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/18/2022] [Revised: 11/12/2022] [Accepted: 12/30/2022] [Indexed: 01/06/2023] Open
Abstract
Streptococcus pneumoniae (SP) is associated with lung cancer, yet its role in the tumorigenesis remains uncertain. Herein we find that SP attaches to lung cancer cells via binding pneumococcal surface protein C (PspC) to platelet-activating factor receptor (PAFR). Interaction between PspC and PAFR stimulates cell proliferation and activates PI3K/AKT and nuclear factor kB (NF-kB) signaling pathways, which trigger a pro-inflammatory response. Lung cancer cells infected with SP form larger tumors in BALB/C mice compared to untreated cells. Mice treated with tobacco carcinogen and SP develop more lung tumors and had shorter survival period than mice treated with the carcinogen alone. Mutating PspC or PAFR abolishes tumor-promoting effects of SP. Overabundance of SP is associated with the survival. SP may play a driving role in lung tumorigenesis by activating PI3K/AKT and NF-kB pathways via binding PspC to PAFR and provide a microbial target for diagnosis and treatment of the disease.
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Affiliation(s)
- Ning Li
- Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA
- Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Huifen Zhou
- Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Van K. Holden
- Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Janaki Deepak
- Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Pushpa Dhilipkannah
- Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Nevins W. Todd
- Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Sanford A. Stass
- Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA
| | - Feng Jiang
- Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA
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10
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Jeong YJ, Kim CU, Lee KS, Kim JH, Park SY, Jeong AY, Lee JB, Kim DJ, Park YJ, Lee MS. Pseudomonas stutzeri PM101005 inhaled with atmospheric particulate matter induces lung damage through inflammatory responses. ENVIRONMENTAL POLLUTION (BARKING, ESSEX : 1987) 2023; 317:120741. [PMID: 36435285 DOI: 10.1016/j.envpol.2022.120741] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/13/2022] [Revised: 11/14/2022] [Accepted: 11/22/2022] [Indexed: 06/16/2023]
Abstract
Atmospheric particulate matter (PM) contains a mixture of chemical and biological elements that pose threat to human health by increasing susceptibility to respiratory diseases. Although the identification of the microorganisms composing the PM has been assessed, their immunological impacts are still questionable. Here, we examined the mechanisms responsible for the pathogenicity of Pseudomonas stutzeri PM101005 (PMPS), a bacterium isolated from fine dust, in lung epithelial cells, alveolar cells, and macrophages. Relative to its comparative strain Pseudomonas stutzeri (PS), infections with PMPS induced higher production of inflammatory cytokines and chemokines, mediated by the activation of NF-κB and MAPK signaling pathways. Additionally, with three-dimensional (3D) airway spheroids which mimic the human bronchial epithelium, we confirmed that PMPS infections lead to relatively higher induction of pro-inflammatory cytokines than PM infections. Consistent results were observed in murine models as the infections with PMPS provoked greater inflammatory responses than the infections with PS. These PMPS-induced responses were mediated by the signaling pathways of the Toll-like receptors (TLRs), which regulated PMPS infection and played an important role in the expression of the antibiotic peptide β-defensin 3 (BD3) that suppressed PMPS proliferation. Moreover, PM pretreatment enhanced inflammatory responses and tissue damage of PMPS, while reducing BD3 expression. Overall, these results indicate that PM-isolated PMPS induce TLR-mediated inflammatory responses in lung tissues, and contributes to the understanding of the etiology of PM-induced respiratory damage.
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Affiliation(s)
- Yu-Jin Jeong
- Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
| | - Chang-Ung Kim
- Infectious Disease Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
| | - Kyung-Soo Lee
- Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea; Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea
| | - Ji Hyung Kim
- Department of Food Science and Biotechnology, Gachon University, Seongnam, 13120, Republic of Korea
| | - Seo Young Park
- Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
| | - Ahn Young Jeong
- Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea; Infectious Disease Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
| | - Jun Bong Lee
- College of Veterinary Medicine & Institute of Veterinary Science, Kangwon National University, Chuncheon, Kangwon, 24341, Republic of Korea
| | - Doo-Jin Kim
- Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea; Infectious Disease Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea
| | - Young-Jun Park
- Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea; Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea
| | - Moo-Seung Lee
- Environmental Diseases Research Center, Korea Research Institute of Bioscience & Biotechnology (KRIBB), 125 Gwahak-ro, Daejeon, 34141, Republic of Korea; Department of Biomolecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), 127 Gajeong-ro, Yuseong-gu, Daejeon, 34113, Republic of Korea.
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11
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Long T, Ye Z, Tang Y, Shi J, Wen J, Chen C, Huo Q. Comparison of bacterial community structure in PM 2.5 during hazy and non-hazy periods in Guilin, South China. AEROBIOLOGIA 2023; 39:87-103. [PMID: 36568442 PMCID: PMC9762634 DOI: 10.1007/s10453-022-09777-0] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 05/31/2022] [Accepted: 12/09/2022] [Indexed: 05/19/2023]
Abstract
UNLABELLED In recent years, significant efforts have been made to study changes in the levels of air pollutants at regional and urban scales, and changes in bioaerosols during air pollution events have attracted increasing attention. In this study, the bacterial structure of PM2.5 was analysed under different environmental conditions during hazy and non-hazy periods in Guilin. A total of 32 PM2.5 samples were collected in December 2020 and July 2021, and the microbial community structures were analysed using high-throughput sequencing methods. The results show that air pollution and climate change alter the species distribution and community diversity of bacteria in PM2.5, particularly Sphingomonas and Pseudomonas. The structure of the bacterial community composition is related to diurnal variation, vertical height, and urban area and their interactions with various environmental factors. This is a comprehensive study that characterises the variability of bacteria associated with PM2.5 in a variety of environments, highlighting the impacts of environmental effects on the atmospheric microbial community. The results will contribute to our understanding of haze trends in China, particularly the relationship between bioaerosol communities and the urban environment. SUPPLEMENTARY INFORMATION The online version contains supplementary material available at 10.1007/s10453-022-09777-0.
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Affiliation(s)
- Tengfa Long
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
| | - Ziwei Ye
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
| | - Yanchun Tang
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
| | - Jiaxin Shi
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
| | - Jianhui Wen
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
- Guilin Ecological Environmental Monitoring Center, Guilin, 541004 China
| | - Chunqiang Chen
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
| | - Qiang Huo
- Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection (Guangxi Normal University), Ministry of Education, Guilin, 541006 China
- College of Environment and Resources, Guangxi Normal University, Guilin, 541006 China
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12
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Chloroform Fraction of Prasiola japonica Ethanolic Extract Alleviates UPM 1648a-Induced Lung Injury by Suppressing NF-κB Signaling. Foods 2022; 12:foods12010088. [PMID: 36613305 PMCID: PMC9818875 DOI: 10.3390/foods12010088] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2022] [Revised: 12/15/2022] [Accepted: 12/21/2022] [Indexed: 12/28/2022] Open
Abstract
Prasiola japonica is an edible alga, and the ethanol extract of P. japonica (Pj-EE) possesses various biological activities. Interestingly, in a recent study, we observed the potent anti-inflammatory activity of the chloroform fraction of Pj-EE (Pj-EE-CF). Thus, to extend the application of Pj-EE-CF, we further studied its effects on lung injury. To establish an experimental model of lung injury, we nasally administered urban particulate matter UPM 1648a (50 mg/kg) to mice. In addition, BEAS-2B cells were treated with 300 μg/mL of UPM 1648a for in vitro analysis. Intranasal administration of UPM 1648a increased lung injury score, macrophage infiltration, and upregulation of the inflammatory enzyme inducible nitric oxide synthase (iNOS) in lung tissues. On the other hand, oral administration of Pj-EE-CF (25, 50, and 100 mg/kg) alleviated these pathological features as assessed by lung wet/dry ratio, lung injury score, bronchoalveolar lavage fluid (BALF) protein amount in the lung tissues up to 70%, 95%, and 99%, respectively. In addition, Pj-EE-CF down-regulated the release of inflammatory cytokines, interleukins (ILs), tumor necrosis factor (TNF)-α, and interferon (IFN)-γ elevated by UPM 1648a in the lung tissues and lung BALF up to 95%. According to Western blot and luciferase assay, Pj-EE-CF (100 mg/kg in vivo or 50 and 100 μg/mL in vitro) significantly reduced the nuclear factor-κB (NF-κB) signal activated by UPM 1648a. Finally, UPM 1648a increased cellular reactive oxygen species (ROS) levels in BEAS-2B cells, while Pj-EE-CF reduced them. These results suggest that Pj-EE-CF alleviates UPM 1648a-induced lung damage via anti-inflammatory and antioxidant activities and by suppressing NF-κB signaling. In conclusion, these observations imply that Pj-EE-CF could be a practical component of food supplements to mitigate air pollution-derived lung damage.
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13
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Qi Y, Chen Y, Yan X, Liu W, Ma L, Liu Y, Ma Q, Liu S. Co-Exposure of Ambient Particulate Matter and Airborne Transmission Pathogens: The Impairment of the Upper Respiratory Systems. ENVIRONMENTAL SCIENCE & TECHNOLOGY 2022; 56:15892-15901. [PMID: 36240448 PMCID: PMC9670849 DOI: 10.1021/acs.est.2c03856] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 05/30/2022] [Revised: 10/04/2022] [Accepted: 10/04/2022] [Indexed: 06/16/2023]
Abstract
Recent evidence has pinpointed the positive relevance between air particulate matter (PM) pollution and epidemic spread. However, there are still significant knowledge gaps in understanding the transmission and infection of pathogens loaded on PMs, for example, the interactions between pathogens and pre-existing atmospheric PM and the health effects of co-exposure on the inhalation systems. Here, we unraveled the interactions between fine particulate matter (FPM) and Pseudomonas aeruginosa (P. aeruginosa) and evaluated the infection and detrimental effects of co-exposure on the upper respiratory systems in both in vitro and in vivo models. We uncovered the higher accessibility and invasive ability of pathogens to epithelial cells after loading on FPMs, compared with the single exposure. Furthermore, we designed a novel laboratory exposure model to simulate a real co-exposure scenario. Intriguingly, the co-exposure induced more serious functional damage and longer inflammatory reactions to the upper respiratory tract, including the nasal cavity and trachea. Collectively, our results provide a new point of view on the transmission and infection of pathogens loaded on FPMs and uncover the in vivo systematic impairments of the inhalation tract under co-exposure through a novel laboratory exposure model. Hence, this study sheds light on further investigations of the detrimental effects of air pollution and epidemic spread.
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Affiliation(s)
- Yu Qi
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Yucai Chen
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Xu Yan
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Wei Liu
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Li Ma
- Aerosol
and Haze Laboratory, Advanced Innovation Center for Soft Matter Science
and Engineering, Beijing University of Chemical
Technology, Beijing 100029, China
| | - Yongchun Liu
- Aerosol
and Haze Laboratory, Advanced Innovation Center for Soft Matter Science
and Engineering, Beijing University of Chemical
Technology, Beijing 100029, China
| | - Qingxin Ma
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
| | - Sijin Liu
- State
Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese
Academy of Sciences, 18 Shuangqing Road, Haidian District, Beijing 100085, China
- College
of Resources and Environment, University
of Chinese Academy of Sciences, Beijing 100049, China
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14
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Beentjes D, Shears RK, French N, Neill DR, Kadioglu A. Mechanistic Insights into the Impact of Air Pollution on Pneumococcal Pathogenesis and Transmission. Am J Respir Crit Care Med 2022; 206:1070-1080. [PMID: 35649181 PMCID: PMC9704843 DOI: 10.1164/rccm.202112-2668tr] [Citation(s) in RCA: 12] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2021] [Accepted: 06/01/2022] [Indexed: 11/16/2022] Open
Abstract
Streptococcus pneumoniae (the pneumococcus) is the leading cause of pneumonia and bacterial meningitis. A number of recent studies indicate an association between the incidence of pneumococcal disease and exposure to air pollution. Although the epidemiological evidence is substantial, the underlying mechanisms by which the various components of air pollution (particulate matter and gases such as NO2 and SO2) can increase susceptibility to pneumococcal infection are less well understood. In this review, we summarize the various effects air pollution components have on pneumococcal pathogenesis and transmission; exposure to air pollution can enhance host susceptibility to pneumococcal colonization by impairing the mucociliary activity of the airway mucosa, reducing the function and production of key antimicrobial peptides, and upregulating an important pneumococcal adherence factor on respiratory epithelial cells. Air pollutant exposure can also impair the phagocytic killing ability of macrophages, permitting increased replication of S. pneumoniae. In addition, particulate matter has been shown to activate various extra- and intracellular receptors of airway epithelial cells, which may lead to increased proinflammatory cytokine production. This increases recruitment of innate immune cells, including macrophages and neutrophils. The inflammatory response that ensues may result in significant tissue damage, thereby increasing susceptibility to invasive disease, because it allows S. pneumoniae access to the underlying tissues and blood. This review provides an in-depth understanding of the interaction between air pollution and the pneumococcus, which has the potential to aid the development of novel treatments or alternative strategies to prevent disease, especially in areas with high concentrations of air pollution.
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Affiliation(s)
- Daan Beentjes
- Department of Clinical Immunology, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom
| | - Rebecca K Shears
- Department of Clinical Immunology, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom
| | - Neil French
- Department of Clinical Immunology, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom
| | - Daniel R Neill
- Department of Clinical Immunology, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom
| | - Aras Kadioglu
- Department of Clinical Immunology, Microbiology and Immunology, University of Liverpool, Liverpool, United Kingdom
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15
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Zhi Y, Chen X, Cao G, Chen F, Seo HS, Li F. The effects of air pollutants exposure on the transmission and severity of invasive infection caused by an opportunistic pathogen Streptococcus pyogenes. ENVIRONMENTAL POLLUTION (BARKING, ESSEX : 1987) 2022; 310:119826. [PMID: 35932897 DOI: 10.1016/j.envpol.2022.119826] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 05/09/2022] [Revised: 06/30/2022] [Accepted: 07/18/2022] [Indexed: 06/15/2023]
Abstract
Currently, urbanization is associated with an increase in air pollutants that contribute to invasive pathogen infections by altering the host's innate immunity and antimicrobial resistance capability. Streptococcus pyogenes, also known as Group A Streptococcus (GAS), is a gram-positive opportunistic pathogen that causes a wide range of diseases, especially in children and immunosuppressed individuals. Diesel exhaust particle (DEP), a significant constituent of particulate matter (PM), are considered a prominent risk factor for respiratory illness and circulatory diseases worldwide. Several clinical and epidemiological studies have identified a close association between PM and the prevalence of viral and bacterial infections. This study investigated the role of DEP exposure in increasing pulmonary and blood bacterial counts and mortality during GAS M1 strain infection in mice. Thus, we characterized the upregulation of reactive oxygen species production and disruption of tight junctions in the A549 lung epithelial cell line due to DEP exposure, leading to the upregulation of GAS adhesion and invasion. Furthermore, DEP exposure altered the leukocyte components of infiltrated cells in bronchoalveolar lavage fluid, as determined by Diff-Quik staining. The results highlighted the DEP-related macrophage dysfunction, neutrophil impairment, and imbalance in pro-inflammatory cytokine production via the toll-like receptor 4/mitogen-activated protein kinase signaling axis. Notably, the tolerance of the GAS biofilms toward potent antibiotics and bacterial resistance against environmental stresses was also significantly enhanced by DEP. This study aimed to provide a better understanding of the physiological and molecular interactions between exposure to invasive air pollutants and susceptibility to invasive GAS infections.
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Affiliation(s)
- Yong Zhi
- Department of Obstetrics and Gynecology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China
| | - Xinyu Chen
- Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-gil, Jeongeup, Jeollabuk-do, 56212, Republic of Korea; Department of Human and Environmental Toxicology, University of Science & Technology, Daejeon, 34113, Republic of Korea
| | - Guangxu Cao
- Department of Obstetrics and Gynecology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China
| | - Fengjia Chen
- Research Division for Radiation Science, Korea Atomic Energy Research Institute, Jeongeup, 56212, Jeollabuk-do, Republic of Korea
| | - Ho Seong Seo
- Research Division for Radiation Science, Korea Atomic Energy Research Institute, Jeongeup, 56212, Jeollabuk-do, Republic of Korea; Department of Radiation Biotechnology and Applied Radioisotope Science, University of Science and Technology, Daejeon, Republic of Korea
| | - Fang Li
- Department of Obstetrics and Gynecology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
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16
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A particulate matter: How environmental irritants and particulate matter increase sensitivity to bacterial respiratory tract infections. Commentary for “Underground railway particulate matter and susceptibility to pneumococcal infection”. EBioMedicine 2022; 81:104116. [PMID: 35728486 PMCID: PMC9218133 DOI: 10.1016/j.ebiom.2022.104116] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/02/2022] [Accepted: 06/07/2022] [Indexed: 11/18/2022] Open
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17
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Miyashita L, Shears R, Foley G, Semple S, Kadioglu A, Grigg J. Underground railway particulate matter and susceptibility to pneumococcal infection. EBioMedicine 2022; 80:104063. [PMID: 35598440 PMCID: PMC9127572 DOI: 10.1016/j.ebiom.2022.104063] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/26/2022] [Revised: 04/26/2022] [Accepted: 04/30/2022] [Indexed: 12/25/2022] Open
Abstract
BACKGROUND Concentrations of particulate matter less than 10 microns (PM10) on underground railways are higher than those near urban roads. Traffic-related PM10 increases pneumococcal infection via increasing the expression of platelet-activating factor receptor (PAFR), a receptor co-opted by pneumococci to adhere to cells. To date, it is unknown whether underground railway PM10 increases pneumococcal infection. This study sought to determine the effect of London Underground (LU) PM10 on; i) pneumococcal adhesion to airway cells, and ii) susceptibility to pneumococcal disease. METHODS A549 cells and human primary airway epithelial cells were cultured with 20 µg/mL PM10 from the Bakerloo (B-PM10) and Jubilee (J-PM10) line platforms of Baker Street station. PAFR expression was assessed by flow cytometry, and pneumococcal adhesion by colony forming unit (CFU) counts. Traffic-related PM10 was collected next to a main road near the station's entrance. The PAFR blocker CV3988 and the antioxidant N-acetyl cysteine were used to assess the role of PAFR-mediated pneumococcal adhesion and oxidative stress respectively. Pneumococcal infection of mice was done after exposure to 3×80 μg doses of intranasal LU-PM10. FINDINGS In A549 cells, human primary nasal cells, and human primary bronchial epithelial cells, B-PM10 and J-PM10 increased PAFR expression and pneumococcal adhesion. Stimulated adhesion was abrogated by CV3988 and N-acetyl cysteine. Traffic-related PM10 stimulated increased adhesion compared with B-PM10. B-PM10 and J-PM10 increased lung and blood CFU and mortality in mice. Treatment of B-PM10-exposed mice with CV3988 reduced blood CFU. INTERPRETATION LU-PM10 increases pneumococcal adhesion to airway cells and susceptibility to invasive disease in mice. FUNDING The Medical College of Saint Bartholomew's Hospital Trust, and the UK Medical Research Council Programme Grant (MR/P011284/1).
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Affiliation(s)
- Lisa Miyashita
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK
| | - Rebecca Shears
- The Department of Clinical Infection, Microbiology and Immunology, University of Liverpool, Liverpool, UK
| | - Gary Foley
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK
| | - Sean Semple
- Institute for Social Marketing and Health, University of Stirling, Scotland
| | - Aras Kadioglu
- The Department of Clinical Infection, Microbiology and Immunology, University of Liverpool, Liverpool, UK
| | - Jonathan Grigg
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
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18
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Stankovic M, Veljovic K, Popovic N, Kojic S, Dunjic Manevski S, Radojkovic D, Golic N. Lactobacillus brevis BGZLS10-17 and Lb. plantarum BGPKM22 Exhibit Anti-Inflammatory Effect by Attenuation of NF-κB and MAPK Signaling in Human Bronchial Epithelial Cells. Int J Mol Sci 2022; 23:5547. [PMID: 35628361 PMCID: PMC9146699 DOI: 10.3390/ijms23105547] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/23/2022] [Revised: 05/12/2022] [Accepted: 05/12/2022] [Indexed: 12/28/2022] Open
Abstract
Bronchial epithelial cells are exposed to environmental influences, microbiota, and pathogens and also serve as a powerful effector that initiate and propagate inflammation by the release of pro-inflammatory mediators. Recent studies suggested that lung microbiota differ between inflammatory lung diseases and healthy lungs implicating their contribution in the modulation of lung immunity. Lactic acid bacteria (LAB) are natural inhabitants of healthy human lungs and also possess immunomodulatory effects, but so far, there are no studies investigating their anti-inflammatory potential in respiratory cells. In this study, we investigated immunomodulatory features of 21 natural LAB strains in lipopolysaccharide (LPS)-stimulated human bronchial epithelial cells (BEAS-2B). Our results show that several LAB strains reduced the expression of pro-inflammatory cytokine and chemokine genes. We also demonstrated that two LAB strains, Lactobacillus brevis BGZLS10-17 and Lb. plantarum BGPKM22, effectively attenuated LPS-induced nuclear factor-κB (NF-κB) nuclear translocation. Moreover, BGZLS10-17 and BGPKM22 reduced the activation of p38, extracellular signal-related kinase (ERK), and c-Jun amino-terminal kinase (JNK) signaling cascade resulting in a reduction of pro-inflammatory mediator expressions in BEAS-2B cells. Collectively, the LAB strains BGZLS10-17 and BGPKM22 exhibited anti-inflammatory effects in BEAS-2B cells and could be employed to balance immune response in lungs and replenish diminished lung microbiota in chronic lung diseases.
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Affiliation(s)
- Marija Stankovic
- Laboratory for Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (S.K.); (S.D.M.); (D.R.)
| | - Katarina Veljovic
- Laboratory for Molecular Microbiology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (K.V.); (N.P.); (N.G.)
| | - Nikola Popovic
- Laboratory for Molecular Microbiology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (K.V.); (N.P.); (N.G.)
| | - Snezana Kojic
- Laboratory for Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (S.K.); (S.D.M.); (D.R.)
| | - Sofija Dunjic Manevski
- Laboratory for Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (S.K.); (S.D.M.); (D.R.)
| | - Dragica Radojkovic
- Laboratory for Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (S.K.); (S.D.M.); (D.R.)
| | - Natasa Golic
- Laboratory for Molecular Microbiology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia; (K.V.); (N.P.); (N.G.)
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19
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Mousavi SE, Delgado-Saborit JM, Adivi A, Pauwels S, Godderis L. Air pollution and endocrine disruptors induce human microbiome imbalances: A systematic review of recent evidence and possible biological mechanisms. THE SCIENCE OF THE TOTAL ENVIRONMENT 2022; 816:151654. [PMID: 34785217 DOI: 10.1016/j.scitotenv.2021.151654] [Citation(s) in RCA: 44] [Impact Index Per Article: 14.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 08/10/2021] [Revised: 10/26/2021] [Accepted: 11/09/2021] [Indexed: 05/25/2023]
Abstract
A rich body of literature indicates that environmental factors interact with the human microbiome and influence its composition and functions contributing to the pathogenesis of diseases in distal sites of the body. This systematic review examines the scientific evidence on the effect of environmental toxicants, air pollutants and endocrine disruptors (EDCs), on compositional and diversity of human microbiota. Articles from PubMed, Embase, WoS and Google Scholar where included if they focused on human populations or the SHIME® model, and assessed the effects of air pollutants and EDCs on human microbiome. Non-human studies, not written in English and not displaying original research were excluded. The Newcastle-Ottawa Scale was used to assess the quality of individual studies. Results were extracted and presented in tables. 31 studies were selected, including 24 related to air pollutants, 5 related to EDCs, and 2 related to EDC using the SHIME® model. 19 studies focussed on the respiratory system (19), gut (8), skin (2), vaginal (1) and mammary (1) microbiomes. No sufficient number of studies are available to observe a consistent trend for most of the microbiota, except for streptococcus and veillionellales for which 9 out of 10, and 3 out of 4 studies suggest an increase of abundance with exposure to air pollution. A limitation of the evidence reviewed is the scarcity of existing studies assessing microbiomes from individual systems. Growing evidence suggests that exposure to environmental contaminants could change the diversity and abundance of resident microbiota, e.g. in the upper and lower respiratory, gastrointestinal, and female reproductive system. Microbial dysbiosis might lead to colonization of pathogens and outgrowth of pathobionts facilitating infectious diseases. It also might prime metabolic dysfunctions disrupting the production of beneficial metabolites. Further studies should elucidate the role of environmental pollutants in the development of dysbiosis and dysregulation of microbiota-related immunological processes.
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Affiliation(s)
- Sayed Esmaeil Mousavi
- Department of Water and Wastewater Treatment, Water and Wastewater Consulting Engineers (Design & Research), Isfahan, Iran
| | - Juana Maria Delgado-Saborit
- Perinatal Epidemiology, Environmental Health and Clinical Research, School of Medicine, Universitat Jaume I, Castellon, Spain; Environmental Research Group, MRC Centre for Environment and Health, Imperial College London, United Kingdom; School of Geography, Earth & Environmental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
| | - Anna Adivi
- Advanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76201, USA
| | - Sara Pauwels
- Department of Public Health and Primary Care, Centre Environment & Health, KU Leuven, Belgium
| | - Lode Godderis
- Department of Public Health and Primary Care, Centre Environment & Health, KU Leuven, Belgium; IDEWE, External Service for Prevention and Protection at work, Interleuvenlaan 58, 3001 Heverlee, Belgium.
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20
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PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 2022; 2022:3618806. [PMID: 35419163 PMCID: PMC9001082 DOI: 10.1155/2022/3618806] [Citation(s) in RCA: 42] [Impact Index Per Article: 14.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 01/15/2022] [Accepted: 03/24/2022] [Indexed: 12/21/2022]
Abstract
Oxidative stress is defined as the imbalance between reactive oxygen species (ROS) production and the endogenous antioxidant defense system, leading to cellular damage. Asthma is a common chronic inflammatory airway disease. The presence of asthma tends to increase the production of reactive oxygen species (ROS), and the antioxidant system in the lungs is insufficient to mitigate it. Therefore, asthma can lead to an exacerbation of airway hyperresponsiveness and airway inflammation. PM2.5 exposure increases ROS levels. Meanwhile, the accumulation of ROS will further enhance the oxidative stress response, resulting in DNA, protein, lipid, and other cellular and molecular damage, leading to respiratory diseases. An in-depth study on the relationship between oxidative stress and PM2.5-related asthma is helpful to understand the pathogenesis and progression of the disease and provides a new direction for the treatment of the disease. This paper reviews the research progress of oxidative stress in PM2.5-induced asthma as well as highlights the therapeutic potentials of antioxidant approaches in treatment of asthma.
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21
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Aghapour M, Ubags ND, Bruder D, Hiemstra PS, Sidhaye V, Rezaee F, Heijink IH. Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD. Eur Respir Rev 2022; 31:31/163/210112. [PMID: 35321933 PMCID: PMC9128841 DOI: 10.1183/16000617.0112-2021] [Citation(s) in RCA: 90] [Impact Index Per Article: 30.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2021] [Accepted: 11/13/2021] [Indexed: 12/12/2022] Open
Abstract
Chronic exposure to environmental pollutants is a major contributor to the development and progression of obstructive airway diseases, including asthma and COPD. Understanding the mechanisms underlying the development of obstructive lung diseases upon exposure to inhaled pollutants will lead to novel insights into the pathogenesis, prevention and treatment of these diseases. The respiratory epithelial lining forms a robust physicochemical barrier protecting the body from inhaled toxic particles and pathogens. Inhalation of airborne particles and gases may impair airway epithelial barrier function and subsequently lead to exaggerated inflammatory responses and airway remodelling, which are key features of asthma and COPD. In addition, air pollutant-induced airway epithelial barrier dysfunction may increase susceptibility to respiratory infections, thereby increasing the risk of exacerbations and thus triggering further inflammation. In this review, we discuss the molecular and immunological mechanisms involved in physical barrier disruption induced by major airborne pollutants and outline their implications in the pathogenesis of asthma and COPD. We further discuss the link between these pollutants and changes in the lung microbiome as a potential factor for aggravating airway diseases. Understanding these mechanisms may lead to identification of novel targets for therapeutic intervention to restore airway epithelial integrity in asthma and COPD. Exposure to air pollution induces airway epithelial barrier dysfunction through several mechanisms including increased oxidative stress, exaggerated cytokine responses and impaired host defence, which contributes to development of asthma and COPD. https://bit.ly/3DHL1CA
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Affiliation(s)
- Mahyar Aghapour
- Infection Immunology Group, Institute of Medical Microbiology, Infection Control and Prevention, Health Campus Immunology, Infectiology and Inflammation, Otto-von-Guericke University, Magdeburg, Germany.,Immune Regulation Group, Helmholtz Center for Infection Research, Braunschweig, Germany
| | - Niki D Ubags
- Faculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Epalinges, Switzerland
| | - Dunja Bruder
- Infection Immunology Group, Institute of Medical Microbiology, Infection Control and Prevention, Health Campus Immunology, Infectiology and Inflammation, Otto-von-Guericke University, Magdeburg, Germany.,Immune Regulation Group, Helmholtz Center for Infection Research, Braunschweig, Germany
| | - Pieter S Hiemstra
- Dept of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands
| | - Venkataramana Sidhaye
- Pulmonary and Critical Care Medicine, Environmental Health and Engineering, Johns Hopkins University, Baltimore, MD, USA
| | - Fariba Rezaee
- Center for Pediatric Pulmonary Medicine, Cleveland Clinic Children's, Cleveland, OH, USA.,Dept of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
| | - Irene H Heijink
- University of Groningen, University Medical Center Groningen, Depts of Pathology and Medical Biology and Pulmonology, Groningen Research Institute for Asthma and COPD (GRIAC), Groningen, The Netherlands
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22
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Chen H, Du R, Zhang Y, Du P, Zhang S, Ren W, Yang M. Evolution of PM 2.5 bacterial community structure in Beijing's suburban atmosphere. THE SCIENCE OF THE TOTAL ENVIRONMENT 2021; 799:149387. [PMID: 34365268 DOI: 10.1016/j.scitotenv.2021.149387] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/16/2021] [Revised: 07/21/2021] [Accepted: 07/28/2021] [Indexed: 06/13/2023]
Abstract
Biosafety has become one of the greatest challenges facing humanity. Outbreaks of infectious diseases caused by bacteria and viruses have had a huge impact on public health. In addition, non-severe polluted air quality has gradually become the norm; however, literature on the impacts of bioaerosols under long-term exposure to low concentrations of PM2.5 in China is limited. This study analyzed the evolution of the PM2.5 bacterial community in the Huairou district of Beijing under different pollution conditions. We used high-throughput sequencing to seasonally analyze samples over a year (from July 2018 to May 2019) and winter samples from different years (2015, 2016, 2018, and 2019). The results showed that the bacterial diversity and community composition of PM2.5 were significantly different in different seasons, whereas under different pollution levels, there were no significant differences. During the observation period, the number of bacterial species decreased with the increase in pollution; however, a high proportion of bacteria can exist as core species under different pollution levels for a long time. Furthermore, bacteria can be relatively stable in the local environment during the same season but in different years. Although the relative abundances of different bacteria change differently with the variation in pollution level, there is no statistical difference. Importantly, there was a higher abundance of opportunistic pathogenic bacteria when the air quality index was 0-100 in winter. This study comprehensively revealed the characteristics of the evolution of bacterial communities under different pollution levels and in different years and emphasized the health effects of non-pollution air quality. This study can provide a theoretical basis for establishing a sound environmental microbial monitoring and defense system.
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Affiliation(s)
- Hanlin Chen
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
| | - Rui Du
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China.
| | - Yongtao Zhang
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
| | - Pengrui Du
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
| | - Sujian Zhang
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
| | - Weishan Ren
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
| | - Mei Yang
- College of Resources and Environment, University of Chinese Academy of Sciences, Beijing 100049, China
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Cai YS, Gibson H, Ramakrishnan R, Mamouei M, Rahimi K. Ambient Air Pollution and Respiratory Health in Sub-Saharan African Children: A Cross-Sectional Analysis. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2021; 18:ijerph18189729. [PMID: 34574653 PMCID: PMC8467583 DOI: 10.3390/ijerph18189729] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/27/2021] [Revised: 09/11/2021] [Accepted: 09/13/2021] [Indexed: 02/03/2023]
Abstract
Ambient air pollution is projected to become a major environmental risk in sub-Saharan Africa (SSA). Research into its health impacts is hindered by limited data. We aimed to investigate the cross-sectional relationship between particulate matter with a diameter ≤ 2.5 μm (PM2.5) and prevalence of cough or acute lower respiratory infection (ALRI) among children under five in SSA. Data were collected from 31 Demographic and Health Surveys (DHS) in 21 SSA countries between 2005–2018. Prior-month average PM2.5 preceding the survey date was assessed based on satellite measurements and a chemical transport model. Cough and ALRI in the past two weeks were derived from questionnaires. Associations were analysed using conditional logistic regression within each survey cluster, adjusting for child’s age, sex, birth size, household wealth, maternal education, maternal age and month of the interview. Survey-specific odds ratios (ORs) were pooled using random-effect meta-analysis. Included were 368,366 and 109,664 children for the analysis of cough and ALRI, respectively. On average, 20.5% children had reported a cough, 6.4% reported ALRI, and 32% of children lived in urban areas. Prior-month average PM2.5 ranged from 8.9 to 64.6 μg/m3. Pooling all surveys, no associations were observed with either outcome in the overall populations. Among countries with medium-to-high Human Development Index, positive associations were observed with both cough (pooled OR: 1.022, 95%CI: 0.982–1.064) and ALRI (pooled OR: 1.018, 95%CI: 0.975–1.064) for 1 μg/m3 higher of PM2.5. This explorative study found no associations between short-term ambient PM2.5 and respiratory health among young SSA children, necessitating future analyses using better-defined exposure and health metrics to study this important link.
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Affiliation(s)
- Yutong Samuel Cai
- Nuffield Department of Women’s & Reproductive Health, University of Oxford, Oxford OX3 9DU, UK; (H.G.); (M.M.); (K.R.)
- Deep Medicine Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
- Informal Cities Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
- Correspondence:
| | - Harry Gibson
- Nuffield Department of Women’s & Reproductive Health, University of Oxford, Oxford OX3 9DU, UK; (H.G.); (M.M.); (K.R.)
- Deep Medicine Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
- Informal Cities Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
| | - Rema Ramakrishnan
- National Perinatal Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford OX3 7LF, UK;
| | - Mohammad Mamouei
- Nuffield Department of Women’s & Reproductive Health, University of Oxford, Oxford OX3 9DU, UK; (H.G.); (M.M.); (K.R.)
- Deep Medicine Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
- Informal Cities Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
| | - Kazem Rahimi
- Nuffield Department of Women’s & Reproductive Health, University of Oxford, Oxford OX3 9DU, UK; (H.G.); (M.M.); (K.R.)
- Deep Medicine Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
- Informal Cities Programme, Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK
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Niemeier-Walsh C, Ryan PH, Meller J, Ollberding NJ, Adhikari A, Reponen T. Exposure to traffic-related air pollution and bacterial diversity in the lower respiratory tract of children. PLoS One 2021; 16:e0244341. [PMID: 34166366 PMCID: PMC8224880 DOI: 10.1371/journal.pone.0244341] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/03/2020] [Accepted: 05/26/2021] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND Exposure to particulate matter has been shown to increase the adhesion of bacteria to human airway epithelial cells. However, the impact of traffic-related air pollution (TRAP) on the respiratory microbiome is unknown. METHODS Forty children were recruited through the Cincinnati Childhood Allergy and Air Pollution Study, a longitudinal cohort followed from birth through early adolescence. Saliva and induced sputum were collected at age 14 years. Exposure to TRAP was characterized from birth through the time of sample collection using a previously validated land-use regression model. Sequencing of the bacterial 16S and ITS fungal rRNA genes was performed on sputum and saliva samples. The relative abundance of bacterial taxa and diversity indices were compared in children with exposure to high and low TRAP. We also used multiple linear regression to assess the effect of TRAP exposure, gender, asthma status, and socioeconomic status on the alpha diversity of bacteria in sputum. RESULTS We observed higher bacterial alpha diversity indices in sputum than in saliva. The diversity indices for bacteria were greater in the high TRAP exposure group than the low exposure group. These differences remained after adjusting for asthma status, gender, and mother's education. No differences were observed in the fungal microbiome between TRAP exposure groups. CONCLUSION Our findings indicate that exposure to TRAP in early childhood and adolescence may be associated with greater bacterial diversity in the lower respiratory tract. Asthma status does not appear to confound the observed differences in diversity. These results demonstrate that there may be a TRAP-exposure related change in the lower respiratory microbiota that is independent of asthma status.
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Affiliation(s)
- Christine Niemeier-Walsh
- Department of Environmental Health, University of Cincinnati, Cincinnati, OH, United States of America
| | - Patrick H. Ryan
- Department of Environmental Health, University of Cincinnati, Cincinnati, OH, United States of America
- Department of Pediatrics, University of Cincinnati, Cincinnati, OH, United States of America
- Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, United States of America
| | - Jaroslaw Meller
- Department of Environmental Health, University of Cincinnati, Cincinnati, OH, United States of America
- Department of Pediatrics, University of Cincinnati, Cincinnati, OH, United States of America
| | - Nicholas J. Ollberding
- Department of Pediatrics, University of Cincinnati, Cincinnati, OH, United States of America
- Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, United States of America
| | - Atin Adhikari
- Jiann-Ping Hsu College of Public Health, Georgia Southern University, Statesboro, Georgia, United States of America
| | - Tiina Reponen
- Department of Environmental Health, University of Cincinnati, Cincinnati, OH, United States of America
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25
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Misiukiewicz-Stepien P, Paplinska-Goryca M. Biological effect of PM 10 on airway epithelium-focus on obstructive lung diseases. Clin Immunol 2021; 227:108754. [PMID: 33964432 DOI: 10.1016/j.clim.2021.108754] [Citation(s) in RCA: 23] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/24/2020] [Revised: 04/16/2021] [Accepted: 05/03/2021] [Indexed: 12/11/2022]
Abstract
Recently, a continuous increase in environmental pollution has been observed. Despite wide-scale efforts to reduce air pollutant emissions, the problem is still relevant. Exposure to elevated levels of airborne particles increased the incidence of respiratory diseases. PM10 constitute the largest fraction of air pollutants, containing particles with a diameter of less than 10 μm, metals, pollens, mineral dust and remnant material from anthropogenic activity. The natural airway defensive mechanisms against inhaled material, such as mucus layer, ciliary clearance and macrophage phagocytic activity, may be insufficient for proper respiratory function. The epithelium layer can be disrupted by ongoing oxidative stress and inflammatory processes induced by exposure to large amounts of inhaled particles as well as promote the development and exacerbation of obstructive lung diseases. This review draws attention to the current state of knowledge about the physical features of PM10 and its impact on airway epithelial cells, and obstructive pulmonary diseases.
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Affiliation(s)
- Paulina Misiukiewicz-Stepien
- Postgraduate School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland; Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Poland.
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26
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Kamio N, Hayata M, Tamura M, Tanaka H, Imai K. Porphyromonas gingivalis enhances pneumococcal adhesion to human alveolar epithelial cells by increasing expression of host platelet-activating factor receptor. FEBS Lett 2021; 595:1604-1612. [PMID: 33792027 DOI: 10.1002/1873-3468.14084] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/04/2021] [Revised: 03/18/2021] [Accepted: 03/18/2021] [Indexed: 12/30/2022]
Abstract
Streptococcus pneumoniae causes pneumonia by infecting the alveolar epithelium via binding to host receptors, such as the platelet-activating factor receptor (PAFR). Although chronic periodontitis has been identified as a pneumonia risk factor, how periodontopathic bacteria cause pneumonia is not known. We found that S. pneumoniae adhered to PAFR expressed on A549 human alveolar epithelial cells stimulated by Porphyromonas gingivalis culture supernatant, and this was abrogated by a PAFR-specific inhibitor. Among the major virulence factors of P. gingivalis [lipopolysaccharide (LPS), fimbriae and gingipains (Rgps and Kgp)], PAFR expression and pneumococcal adhesion were executed in an Rgp-dependent manner. LPS and fimbriae did not induce PAFR expression. Hence, our findings suggest that P. gingivalis enhances pneumococcal adhesion to human alveoli by inducing PAFR expression and that gingipains are responsible for this.
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Affiliation(s)
- Noriaki Kamio
- Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan
| | - Mayumi Hayata
- Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan
| | - Muneaki Tamura
- Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan
| | - Hajime Tanaka
- Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan
| | - Kenichi Imai
- Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan
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27
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Yee J, Cho YA, Yoo HJ, Yun H, Gwak HS. Short-term exposure to air pollution and hospital admission for pneumonia: a systematic review and meta-analysis. Environ Health 2021; 20:6. [PMID: 33413431 PMCID: PMC7792212 DOI: 10.1186/s12940-020-00687-7] [Citation(s) in RCA: 39] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/14/2020] [Accepted: 12/14/2020] [Indexed: 05/30/2023]
Abstract
BACKGROUND Air pollution is a major issue that poses a health threat worldwide. Although several studies investigated the adverse effects of air pollution on various diseases, few have directly demonstrated the effects on pneumonia. Therefore, we performed a systematic review and meta-analysis on the associations between short-term exposure of air pollutants and hospital admission or emergency room (ER) visit for pneumonia. METHODS A literature search was performed using PubMed, Embase, and Web of Science up to April 10, 2020. Pooled estimates were calculated as % increase with 95% confidence intervals using a random-effects model. A sensitivity analysis using the leave-one-out method and subgroup analysis by region were performed. RESULTS A total of 21 studies were included in the analysis. Every 10 μg/m3 increment in PM2.5 and PM10 resulted in a 1.0% (95% CI: 0.5-1.5) and 0.4% (95% CI: 0.2-0.6) increase in hospital admission or ER visit for pneumonia, respectively. Every 1 ppm increase of CO and 10 ppb increase of NO2, SO2, and O3 was associated with 4.2% (95% CI: 0.6-7.9), 3.2% (95% CI: 1.3-5.1), 2.4% (95% CI: - 2.0-7.1), and 0.4% (95% CI: 0-0.8) increase in pneumonia-specific hospital admission or ER visit, respectively. Except for CO, the sensitivity analyses yielded similar results, demonstrating the robustness of the results. In a subgroup analysis by region, PM2.5 increased hospital admission or ER visit for pneumonia in East Asia but not in North America. CONCLUSION By combining the inconsistent findings of several studies, this study revealed the associations between short-term exposure of air pollutants and pneumonia-specific hospital admission or ER visit, especially for PM and NO2. Based on the results, stricter intervention policies regarding air pollution and programs for protecting human respiratory health should be implemented.
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Affiliation(s)
- Jeong Yee
- College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, Republic of Korea
| | - Young Ah Cho
- College of Pharmacy, Gyeongsang National University, Jinju, Gyeongnam, 52828, Republic of Korea
- Mokhwa Convalescent Hospital, Jinju, Gyeongnam, 52828, Republic of Korea
| | - Hee Jeong Yoo
- College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, Republic of Korea
- Department of Pharmacy, National Medical Center, Seoul, 04564, Republic of Korea
| | - Hyunseo Yun
- Graduate School of Clinical Biohealth, Ewha Womans University, Seoul, 03760, Republic of Korea
| | - Hye Sun Gwak
- College of Pharmacy and Graduate School of Pharmaceutical Sciences, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, Republic of Korea.
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28
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Shahbaz MA, Martikainen MV, Rönkkö TJ, Komppula M, Jalava PI, Roponen M. Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro. ENVIRONMENTAL RESEARCH 2021; 192:110244. [PMID: 32980306 PMCID: PMC7516585 DOI: 10.1016/j.envres.2020.110244] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 07/02/2020] [Revised: 09/09/2020] [Accepted: 09/17/2020] [Indexed: 05/05/2023]
Abstract
Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to explore how exposure to relatively low doses of urban air PM alters innate responses to bacterial and viral stimuli in vitro. We used secondary alveolar epithelial cell line along with monocyte-derived macrophages to replicate innate lung barrier in vitro. Co-cultured cells were first exposed for 24 h to PM2.5-1 (particle aerodynamic diameter between 1 and 2.5 μm) and subsequently for an additional 24 h to lipopolysaccharide (TLR4), polyinosinic-polycytidylic acid (TLR3), and synthetic single-stranded RNA oligoribonucleotides (TLR7/8) to mimic bacterial or viral stimulation. Toxicological endpoints included pro-inflammatory cytokines (IL-8, IL-6, and TNF-α), cellular metabolic activity, and cell cycle phase distribution. We show that cells exposed to PM2.5-1 produced higher levels of pro-inflammatory cytokines following stimulation with bacterial TLR4 ligand than cells exposed to PM2.5-1 or bacterial ligand alone. On the contrary, PM2.5-1 exposure reduced pro-inflammatory responses to viral ligands TLR3 and TLR7/8. Cell cycle analysis indicated that viral ligands induced cell cycle arrest at the G2-M phase. In PM-primed co-cultures, however, they failed to induce the G2-M phase arrest. Contrarily, bacterial stimulation caused a slight increase in cells in the sub-G1 phase but in PM2.5-1 primed co-cultures the effect of bacterial stimulation was masked by PM2.5-1. These findings indicate that PM2.5-1 may alter responses of immune defense differently against bacterial and viral infections. Further studies are required to explain the mechanism of immune modulation caused by PM in altering the susceptibility to respiratory infections.
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Affiliation(s)
- Muhammad Ali Shahbaz
- University of Eastern Finland, Department of Environmental and Biological Sciences, Yliopistonranta 1, P.O. Box 1627, FI-70211, Kuopio, Finland.
| | - Maria-Viola Martikainen
- University of Eastern Finland, Department of Environmental and Biological Sciences, Yliopistonranta 1, P.O. Box 1627, FI-70211, Kuopio, Finland
| | - Teemu J Rönkkö
- University of Eastern Finland, Department of Environmental and Biological Sciences, Yliopistonranta 1, P.O. Box 1627, FI-70211, Kuopio, Finland
| | - Mika Komppula
- Finnish Meteorological Institute, Yliopistonranta 1F, P.O. Box 1627, FI-70211, Kuopio, Finland
| | - Pasi I Jalava
- University of Eastern Finland, Department of Environmental and Biological Sciences, Yliopistonranta 1, P.O. Box 1627, FI-70211, Kuopio, Finland
| | - Marjut Roponen
- University of Eastern Finland, Department of Environmental and Biological Sciences, Yliopistonranta 1, P.O. Box 1627, FI-70211, Kuopio, Finland
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Pompilio A, Di Bonaventura G. Ambient air pollution and respiratory bacterial infections, a troubling association: epidemiology, underlying mechanisms, and future challenges. Crit Rev Microbiol 2020; 46:600-630. [PMID: 33059504 DOI: 10.1080/1040841x.2020.1816894] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
The World Health Organization attributed more than four million premature deaths to ambient air pollution in 2016. Numerous epidemiologic studies demonstrate that acute respiratory tract infections and exacerbations of pre-existing chronic airway diseases can result from exposure to ambient (outdoor) air pollution. In this context, the atmosphere contains both chemical and microbial pollutants (bioaerosols), whose impact on human health remains unclear. Therefore, this review: summarises the findings from recent studies on the association between exposure to air pollutants-especially particulate matter and ozone-and onset or exacerbation of respiratory infections (e.g. pneumonia, cystic fibrosis lung infection, and tuberculosis); discusses the mechanisms underlying the relationship between air pollution and respiratory bacterial infections, which is necessary to define prevention and treatment strategies; demonstrates the relevance of air pollution modelling in investigating and preventing the impact of exposure to air pollutants on human health; and outlines future actions required to improve air quality and reduce morbidity and mortality related to air pollution.
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Affiliation(s)
- Arianna Pompilio
- Department of Medical, Oral and Biotechnological Sciences, and Center for Advanced Studies and Technology (CAST), "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy
| | - Giovanni Di Bonaventura
- Department of Medical, Oral and Biotechnological Sciences, and Center for Advanced Studies and Technology (CAST), "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy
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30
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Rouadi PW, Idriss SA, Naclerio RM, Peden DB, Ansotegui IJ, Canonica GW, Gonzalez-Diaz SN, Rosario Filho NA, Ivancevich JC, Hellings PW, Murrieta-Aguttes M, Zaitoun FH, Irani C, Karam MR, Bousquet J. Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD). World Allergy Organ J 2020; 13:100467. [PMID: 33042360 PMCID: PMC7534666 DOI: 10.1016/j.waojou.2020.100467] [Citation(s) in RCA: 24] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2020] [Revised: 08/31/2020] [Accepted: 09/11/2020] [Indexed: 12/14/2022] Open
Abstract
Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases (IAD) such as allergic rhinitis (AR), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disease (COPD). Oxidative stress in patients with IAD can induce eosinophilic inflammation in the airways, augment atopic allergic sensitization, and increase susceptibility to infection. We reviewed emerging data depicting the involvement of oxidative stress in IAD patients. We evaluated biomarkers, outcome measures and immunopathological alterations across the airway mucosal barrier following exposure, particularly when accentuated by an infectious insult.
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Key Words
- AR, Allergic rhinitis
- Air pollution
- Antioxidant
- COPD, Chronic obstructive pulmonary disease
- CRS, Chronic rhinosinusitis
- DEP, Diesel exhaust particles
- IAD, Inflammatory airway diseases
- IL, Interleukin
- ILC, Innate lymphoid cells
- Inflammatory airway disease
- NOx, Nitrogen oxides
- Oxidative stress biomarkers
- PAH, Polycyclic aromatic hydrocarbons
- PM, Particulate matter
- ROS, Reactive oxygen species
- TBS, Tobacco smoke
- TLR, Toll-like receptors
- Tobacco smoke
- Treg, Regulatory T cell
- VOCs, Volatile organic compounds
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Affiliation(s)
- Philip W. Rouadi
- Department of Otolaryngology-Head and Neck Surgery, Eye and Ear University Hospital, Beirut, Lebanon
| | - Samar A. Idriss
- Department of Otolaryngology-Head and Neck Surgery, Eye and Ear University Hospital, Beirut, Lebanon
| | - Robert M. Naclerio
- Johns Hopkins University Department of Otolaryngology - Head and Neck Surgery, Baltimore, MD, USA
| | - David B. Peden
- UNC Center for Environmental Medicine, Asthma, and Lung Biology, Division of Allergy, Immunology and Rheumatology, Department of Pediatrics UNS School of Medicine, USA
| | - Ignacio J. Ansotegui
- Department of Allergy and Immunology, Hospital Quironsalud Bizkaia, Bilbao, Spain
| | | | - Sandra Nora Gonzalez-Diaz
- University Autonoma de Nuevo Leon Facultad de Medicina y Hospital Universitario U.A.N.L, Monterrey, NL, c.p. 64460, México
| | | | - Juan Carlos Ivancevich
- Faculty of Medicine, Universidad del Salvador, Buenos Aires, Argentina and Head of Allergy and Immunology at the Santa Isabel Clinic, Buenos Aires, Argentina
| | - Peter W. Hellings
- Department of Otorhinolaryngology, University Hospitals Leuven, Leuven, Belgium
- Department of Otorhinolaryngology, Academic Medical Center Amsterdam, The Netherlands - Department Otorhinolaryngology, University Hospital Ghent, Belgium
| | | | - Fares H. Zaitoun
- LAUMC Rizk Hospital, Otolaryngology-Allergy Department, Beirut, Lebanon
| | - Carla Irani
- Department of Internal Medicine and Infectious Diseases, St Joseph University, Hotel Dieu de France Hospital, Beirut, Lebanon
| | - Marilyn R. Karam
- Division of Rheumatology, Allergy and Clinical Immunology, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon
| | - Jean Bousquet
- INSERM U 1168, VIMA: Ageing and Chronic Diseases Epidemiological and Public Health Approaches, Villejuif, France
- University Versailles St-Quentin-en-Yvelines, France
- Allergy-Centre-Charité, Charité–Universitätsmedizin Berlin, Berlin, Germany
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31
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Liu J, Chen X, Zhou J, Ye L, Yang D, Song Y. Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via the ROS-mediated PI3K pathway. Hum Cell 2020; 33:963-973. [PMID: 32627147 DOI: 10.1007/s13577-020-00378-y] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2019] [Accepted: 05/14/2020] [Indexed: 11/30/2022]
Abstract
Over exposure to particulate matter (PM) could irritate respiratory tract infection; while, Pseudomonas aeruginosa (P. aeruginosa) is one of the main common pathogens. Our study aims are to define whether PM exposure enhances the invasion of P. aeruginosa into the airway epithelia and to characterize the underlying mechanisms. Human bronchial epithelial cells (BEAS-2B) or BEAS-2B transfected by PAFR siRNA were challenged with PM and pretreated with N-acetylcysteine (NAC), LY294002 (PI3K inhibitor), BAY 11-7082 (NF-κB inhibitor), or CV-3988 (PAFR antagonist). P. aeruginosa invasion was evaluated using colony-forming units assay and confocal microscopy. Real-time RT-PCR, immunofluorescence, flow cytometry and western blotting were used to detect the genes or proteins expression. PM exposure promoted P. aeruginosa invasion into BEAS-2B cells through ROS-mediated PI3K pathway which enhanced the expression of PAFR, which could be alleviated by treatment with NAC, LY294002, and BAY 11-7082. Furthermore, NAC and PAFR siRNA attenuated PM-stimulated activation of PI3K pathway. Treatment with PAFR antagonist and siRNA also alleviated PM exposure-induced P. aeruginosa invasion into BEAS-2B cells. Our results demonstrated that PM exposure increased the PAFR expression and activated the PI3K pathway in a ROS-dependent manner. Upregulated PAFR and activated PI3K pathway formed a positive regulatory loop and promoted the invasion of P. aeruginosa into airway epithelia. These mechanisms may provide a novel approach against P.aeruginosa invasion.
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Affiliation(s)
- Jinguo Liu
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Xiaoyan Chen
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Jian Zhou
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Ling Ye
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Dong Yang
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
| | - Yuanlin Song
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. .,Department of Respiratory Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People's Republic of China. .,Department of Pulmonary Medicine, Zhongshan Hospital, Qingpu Branch, Shanghai, People's Republic of China.
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32
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Zhang S, Huo X, Li M, Hou R, Cong X, Xu X. Oral antimicrobial activity weakened in children with electronic waste lead exposure. ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH INTERNATIONAL 2020; 27:14763-14770. [PMID: 32056098 DOI: 10.1007/s11356-020-08037-3] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/19/2019] [Accepted: 02/10/2020] [Indexed: 02/05/2023]
Abstract
Environmental lead (Pb) exposure can induce dysbacteriosis, impair oral health, and is associated with the development of dental caries. However, the mechanism is unclear. The aim of this study was to explore the effects of Pb toxicity on oral antimicrobial activity in children in an e-waste area. Results showed higher blood Pb levels in e-waste-exposed group children, accompanied by decreased saliva SAG (salivary agglutinin) concentrations, increased peripheral WBC (white blood cell) counts and monocyte counts, and elevated peripheral monocyte percentage. LnPb (natural logarithmic transformation of blood Pb level) was negatively correlated with saliva SAG concentration, while positively correlated with peripheral monocyte percentage. Saliva SAG concentration played a complete mediating role in the correlation of LnPb to peripheral monocyte percentage. To our knowledge, this is the first study on the relationship of environmental Pb exposure and oral antimicrobial activity in children, showing that environmental Pb exposure may weaken oral antimicrobial activity through reducing saliva SAG concentration, which may raise the risk of oral dysbacteriosis and ultimately pathogen infection.
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Affiliation(s)
- Shaocheng Zhang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, 22 Xinling Rd, Shantou, 515041, Guangdong, China
| | - Xia Huo
- Laboratory of Environmental Medicine and Developmental Toxicology, Guangdong Key Laboratory of Environmental Pollution and Health, School of Environment, Jinan University, Guangzhou, 511486, Guangdong, China
| | - Minghui Li
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, 22 Xinling Rd, Shantou, 515041, Guangdong, China
- Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands
| | - Ruikun Hou
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, 22 Xinling Rd, Shantou, 515041, Guangdong, China
| | - Xiaowei Cong
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, 22 Xinling Rd, Shantou, 515041, Guangdong, China
- Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands
| | - Xijin Xu
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, 22 Xinling Rd, Shantou, 515041, Guangdong, China.
- Department of Cell Biology and Genetics, Shantou University Medical College, Shantou, 515041, Guangdong, China.
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33
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Yang L, Li C, Tang X. The Impact of PM 2.5 on the Host Defense of Respiratory System. Front Cell Dev Biol 2020; 8:91. [PMID: 32195248 PMCID: PMC7064735 DOI: 10.3389/fcell.2020.00091] [Citation(s) in RCA: 127] [Impact Index Per Article: 25.4] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2019] [Accepted: 02/04/2020] [Indexed: 12/18/2022] Open
Abstract
The harm of fine particulate matter (PM2.5) to public health is the focus of attention around the world. The Global Burden of Disease (GBD) Study 2015 (GBD 2015 Risk Factors Collaborators, 2016) ranked PM2.5 as the fifth leading risk factor for death, which caused 4.2 million deaths and 103.1 million disability-adjusted life-years (DALYs) loss, representing 7.6% of total global deaths and 4.2% of global DALYs. Epidemiological studies have confirmed that exposure to PM2.5 increases the incidence and mortality of respiratory infections. The host defense dysfunction caused by PM2.5 exposure may be the key to the susceptibility of respiratory system infection. Thus, this review aims to assess the impact of PM2.5 on the host defense of respiratory system. Firstly, we elaborated the epidemiological evidence that exposure to PM2.5 increases the risk of respiratory infections. Secondly, we summarized the experimental evidence that PM2.5 exposure increases the susceptibility of different pathogens (including bacteria and viruses) in respiratory system. Furthermore, here we discussed the underlying host defense mechanisms by which PM2.5 exposure increases the risk of respiratory infections as well as future perspectives.
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Affiliation(s)
- Liyao Yang
- State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
| | - Cheng Li
- State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
| | - Xiaoxiao Tang
- State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
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34
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Ni Y, Shi G, Qu J. Indoor PM 2.5, tobacco smoking and chronic lung diseases: A narrative review. ENVIRONMENTAL RESEARCH 2020; 181:108910. [PMID: 31780052 DOI: 10.1016/j.envres.2019.108910] [Citation(s) in RCA: 63] [Impact Index Per Article: 12.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/03/2019] [Revised: 11/05/2019] [Accepted: 11/07/2019] [Indexed: 06/10/2023]
Abstract
The lung is one of the most important organs exposed to environmental agents. People spend approximately 90% of their time indoors, and risks to health may thus be greater from exposure to poor air quality indoors than outdoors. Multiple indoor pollutants have been linked to chronic respiratory diseases. Environmental tobacco smoke (ETS) is known as an important source of multiple pollutants, especially in indoor environments. Indoor PM2.5 (particulate matter with aerodynamic diameter < 2.5 μm) was reported to be the most reliable marker of the presence of tobacco smoke. Recent studies have demonstrated that PM2.5 is closely correlated with chronic lung diseases. In this paper, we reviewed the relationship of tobacco smoking and indoor PM2.5 and the mechanism that underpin the link of tobacco smoke, indoor PM2.5 and chronic lung diseases.
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Affiliation(s)
- Yingmeng Ni
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Guochao Shi
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Jieming Qu
- Department of Pulmonary and Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Institute of Respiratory Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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35
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Orihuela CJ, Maus UA, Brown JS. Can animal models really teach us anything about pneumonia? Pro. Eur Respir J 2020; 55:55/1/1901539. [DOI: 10.1183/13993003.01539-2019] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/02/2019] [Accepted: 10/03/2019] [Indexed: 01/03/2023]
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36
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Bhalla M, Hui Yeoh J, Lamneck C, Herring SE, Tchalla EYI, Heinzinger LR, Leong JM, Bou Ghanem EN. A1 adenosine receptor signaling reduces Streptococcus pneumoniae adherence to pulmonary epithelial cells by targeting expression of platelet-activating factor receptor. Cell Microbiol 2019; 22:e13141. [PMID: 31709673 DOI: 10.1111/cmi.13141] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2019] [Revised: 10/24/2019] [Accepted: 11/01/2019] [Indexed: 12/11/2022]
Abstract
Extracellular adenosine production is crucial for host resistance against Streptococcus pneumoniae (pneumococcus) and is thought to affect antibacterial immune responses by neutrophils. However, whether extracellular adenosine alters direct host-pathogen interaction remains unexplored. An important determinant for lung infection by S. pneumoniae is its ability to adhere to the pulmonary epithelium. Here we explored whether extracellular adenosine can directly impact bacterial adherence to lung epithelial cells. We found that signaling via A1 adenosine receptor significantly reduced the ability of pneumococci to bind human pulmonary epithelial cells. A1 receptor signaling blocked bacterial binding by reducing the expression of platelet-activating factor receptor, a host protein used by S. pneumoniae to adhere to host cells. In vivo, A1 was required for control of pneumococcal pneumonia as inhibiting it resulted in increased host susceptibility. As S. pneumoniae remain a leading cause of community-acquired pneumonia in the elderly, we explored the role of A1 in the age-driven susceptibility to infection. We found no difference in A1 pulmonary expression in young versus old mice. Strikingly, triggering A1 signaling boosted host resistance of old mice to S. pneumoniae pulmonary infection. This study demonstrates a novel mechanism by which extracellular adenosine modulates resistance to lung infection by targeting bacterial-host interactions.
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Affiliation(s)
- Manmeet Bhalla
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
| | - Jun Hui Yeoh
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
| | - Claire Lamneck
- Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts
| | - Sydney E Herring
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
| | - Essi Y I Tchalla
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
| | - Lauren R Heinzinger
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
| | - John M Leong
- Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts
| | - Elsa N Bou Ghanem
- Department of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York
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37
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Hsieh FC, Huang CY, Lin SF, Sun JT, Yen TH, Chang CC. Short-term exposure to particulate matters is associated with septic emboli in infective endocarditis. Medicine (Baltimore) 2019; 98:e17899. [PMID: 31702666 PMCID: PMC6855621 DOI: 10.1097/md.0000000000017899] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/28/2019] [Revised: 06/17/2019] [Accepted: 10/11/2019] [Indexed: 12/21/2022] Open
Abstract
This survey was to investigate the short-term effect of particulate matters (PMs) exposure on clinical and microbiological variables, especially septic emboli, in infective endocarditis (IE). The study analyzed 138 IE patients in Far Eastern Memorial Hospital from 2005 to 2015 and clinical variables were retrospectively requested. The data of air quality were recorded and collected by a network of 26 monitoring stations spreading in Northern part of Taiwan. We found that IE patients with septic emboli were found to be exposed to a significantly higher level of PM2.5 (32.01 ± 15.89 vs. 21.70 ± 13.05 μg/m, P < .001) and PM10 (54.57 ± 24.43 vs 40.98 ± 24.81 μg/m, P = .002) on lag 0 day when compared to those without. Furthermore, multivariate regression analysis revealed that that ambient exposure to PM2.5 (odds ratio: 3.87, 95% confidence interval: 1.31-8.31; P = .001) and PM10 (odds ratio: 4.58, 95% confidence interval: 2.03-10.32; P < .001) significantly increased risk of septic emboli in IE patients. To our knowledge, this is the first study demonstrating that short-term exposure to PMs was associated with septic emboli in IE.
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Affiliation(s)
- Fu-Chien Hsieh
- Division of Cardiovascular Surgery, Cardiovascular Center
| | | | - Sheng-Feng Lin
- Department of Clinical Pathology, Far Eastern Memorial Hospital, New Taipei
| | | | - Tzung-Hai Yen
- Department of Nephrology and Clinical Poison Center, Chang Gung Memorial Hospital and College of Medicine, Chang Gung University
- Kidney Research Center
- Center for Tissue Engineering, Chang Gung Memorial Hospital, Linkou, Taiwan
| | - Chih-Chun Chang
- Department of Clinical Pathology, Far Eastern Memorial Hospital, New Taipei
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38
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Zhang S, Huo X, Zhang Y, Lu X, Xu C, Xu X. The association of PM 2.5 with airway innate antimicrobial activities of salivary agglutinin and surfactant protein D. CHEMOSPHERE 2019; 226:915-923. [PMID: 31509921 DOI: 10.1016/j.chemosphere.2019.04.032] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 01/09/2019] [Revised: 04/04/2019] [Accepted: 04/04/2019] [Indexed: 02/05/2023]
Abstract
Fine particulate matter ≤2.5 μm (PM2.5) is a prominent global public health risk factor that can cause respiratory infection by downregulating the amounts of antimicrobial proteins and peptides (AMPs). Both salivary agglutinin (SAG) and surfactant protein D (SPD) are important AMPs in respiratory mucosal fluid, providing protection against airway pathogen invasion and infection by inducing microbial aggregation and enhancing pathogen clearance. However, the relationship between PM2.5 and these AMPs is unclear. To better understand the relationship between PM2.5 and airway innate immune defenses, we review the respiratory antimicrobial activities of SAG and SPD, as well as the adverse effects of PM2.5 on airway innate antimicrobial defense. We speculate there exists a dual effect between PM2.5 and respiratory antimicrobial activity, which means that PM2.5 suppresses respiratory antimicrobial activity through downregulating airway AMPs, while airway AMPs accelerate PM2.5 clearance by inducing PM2.5 microbial aggregation. We propose further research on the relationship between PM2.5 and these AMPs.
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Affiliation(s)
- Shaocheng Zhang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou, 515041, Guangdong, China
| | - Xia Huo
- Laboratory of Environmental Medicine and Developmental Toxicology, Guangdong Key Laboratory of Environmental Pollution and Health, School of Environment, Jinan University, Guangzhou, 511486, Guangdong, China
| | - Yuling Zhang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou, 515041, Guangdong, China
| | - Xueling Lu
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou, 515041, Guangdong, China
| | - Cheng Xu
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou, 515041, Guangdong, China
| | - Xijin Xu
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou, 515041, Guangdong, China; Department of Cell Biology and Genetics, Shantou University Medical College, Shantou, 515041, Guangdong, China.
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39
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Zhang S, Huo X, Zhang Y, Huang Y, Zheng X, Xu X. Ambient fine particulate matter inhibits innate airway antimicrobial activity in preschool children in e-waste areas. ENVIRONMENT INTERNATIONAL 2019; 123:535-542. [PMID: 30622078 DOI: 10.1016/j.envint.2018.12.061] [Citation(s) in RCA: 38] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 07/21/2018] [Revised: 12/12/2018] [Accepted: 12/28/2018] [Indexed: 02/05/2023]
Abstract
Ambient fine particulate matter (PM2.5) is a risk factor for respiratory diseases. Previous studies suggest that PM2.5 exposure may down-regulate airway antimicrobial proteins and peptides (AMPs), thereby accelerating airway pathogen infection. However, epidemiological research is scarce. Hence, we estimated the associations between individual PM2.5 chronic daily intake (CDI) and the levels of the airway AMP salivary agglutinin (SAG), as well as peripheral leukocyte counts and pro-inflammatory cytokines, of preschool children in Guiyu (an e-waste area) and Haojiang (a reference area located 31.6 km to the east of Guiyu). We recruited 581 preschool children from Guiyu and Haojiang, of which 222 were included in this study for a matching design (Guiyu: n = 110 vs. Haojiang: n = 112). Air PM2.5 pollution data was collected to calculate individual PM2.5 CDI. The mean concentration of PM2.5 in Guiyu was higher than in Haojiang, resulting in a higher individual PM2.5 CDI. Concomitantly, saliva SAG levels were lower in Guiyu children (5.05 ng/mL) than in Haojiang children (8.68 ng/mL), and were negatively correlated with CDI. Additionally, peripheral counts of white blood cells, and the concentrations of interleukin-8 and tumor necrosis factor-alpha, in Guiyu children were greater than in Haojiang children, and were positively associated with CDI. Similar results were found for neutrophils and monocytes. To our knowledge, this is the first study on the relationship between PM2.5 exposure and innate airway antimicrobial activity in children, in an e-waste area, showing that PM2.5 pollution may weaken airway antimicrobial activity by down-regulation of saliva SAG levels, which might accelerate airway pathogen infection in children.
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Affiliation(s)
- Shaocheng Zhang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou 515041, Guangdong, China
| | - Xia Huo
- Laboratory of Environmental Medicine and Developmental Toxicology, Guangdong Key Laboratory of Environmental Pollution and Health, School of Environment, Jinan University, Guangzhou 511486, Guangdong, China
| | - Yu Zhang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou 515041, Guangdong, China; Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen 9713, GZ, the Netherlands
| | - Yu Huang
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou 515041, Guangdong, China
| | - Xiangbin Zheng
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou 515041, Guangdong, China
| | - Xijin Xu
- Laboratory of Environmental Medicine and Developmental Toxicology, Shantou University Medical College, Shantou 515041, Guangdong, China; Department of Cell Biology and Genetics, Shantou University Medical College, Shantou 515041, Guangdong, China.
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40
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Rajendra KC, Zosky GR, Shukla SD, O’Toole RF. A cost-effective technique for generating preservable biomass smoke extract and measuring its effect on cell receptor expression in human bronchial epithelial cells. Biol Methods Protoc 2018; 3:bpy010. [PMID: 32161803 PMCID: PMC6994070 DOI: 10.1093/biomethods/bpy010] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/10/2018] [Revised: 08/02/2018] [Accepted: 08/10/2018] [Indexed: 12/13/2022] Open
Abstract
Nearly half of the world’s population uses biomass fuel for the purposes of cooking and heating. Smoke derived from biomass increases the risk of the development of lung diseases, including pneumonia, chronic obstructive pulmonary disease, airway tract infections, and lung cancer. Despite the evidence linking biomass smoke exposure to pulmonary disease, only a small number of experimental studies have been conducted on the impact of biomass smoke on airway epithelial cells. This is in part due to the lack of a standard and easily accessible procedure for the preparation of biomass smoke. Here, we describe a cost-effective and reproducible method for the generation of different smoke extracts, in particular, cow dung smoke extract (CDSE) and wood smoke extract (WSE) for use in a range of biological applications. We examined the effect of the biomass smoke extracts on human bronchial epithelial cell expression of a known responder to cigarette smoke exposure (CSE), the platelet-activating factor receptor (PAFR). Similar to the treatment with CSE, we observed a dose-dependent increase in PAFR expression on human airway epithelial cells that were exposed to CDSE and WSE. This method provides biomass smoke in a re-usable form for cell and molecular bioscience studies on the pathogenesis of chronic lung disease.
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Affiliation(s)
- K C Rajendra
- College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
| | - Graeme R Zosky
- College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
| | - Shakti D Shukla
- School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia
| | - Ronan F O’Toole
- College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
- Correspondence address: School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, TAS 7000, Australia. Tel: +61-3-62266974; E-mail:
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41
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Grigg J. Air Pollution and Respiratory Infection: An Emerging and Troubling Association. Am J Respir Crit Care Med 2018; 198:700-701. [DOI: 10.1164/rccm.201804-0614ed] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Affiliation(s)
- Jonathan Grigg
- Centre for Child HealthQueen Mary University of LondonLondon, United Kingdom
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42
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Caruso M, Emma R, Fuochi V, Furneri PM, Polosa R. Electronic cigarette vapour enhances pneumococcal adherence to airway epithelial cells under abnormal conditions of exposure. Eur Respir J 2018; 52:52/3/1800915. [PMID: 30190260 DOI: 10.1183/13993003.00915-2018] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2018] [Accepted: 05/16/2018] [Indexed: 11/05/2022]
Affiliation(s)
- Massimo Caruso
- Dept of Clinical and Experimental Medicine (MEDCLIN), University of Catania, Catania, Italy
| | - Rosalia Emma
- Dept of Clinical and Experimental Medicine (MEDCLIN), University of Catania, Catania, Italy
| | - Virginia Fuochi
- Dept of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
| | - Pio M Furneri
- Dept of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.,Center of Excellence for the Acceleration of Harm Reduction (CoEHAR), University of Catania, Catania, Italy
| | - Riccardo Polosa
- Dept of Clinical and Experimental Medicine (MEDCLIN), University of Catania, Catania, Italy.,Center of Excellence for the Acceleration of Harm Reduction (CoEHAR), University of Catania, Catania, Italy
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43
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Grigg J. Response to: Electronic cigarette vapour enhances pneumococcal adherence to airway epithelial cells under abnormal conditions of exposure. Eur Respir J 2018; 52:52/3/1801199. [PMID: 30190262 DOI: 10.1183/13993003.01199-2018] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/27/2018] [Accepted: 06/27/2018] [Indexed: 11/05/2022]
Affiliation(s)
- Jonathan Grigg
- Centre for Paediatrics, Queen Mary University London, London, UK
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44
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Brugha R, Edmondson C, Davies JC. Outdoor air pollution and cystic fibrosis. Paediatr Respir Rev 2018; 28:80-86. [PMID: 29793860 DOI: 10.1016/j.prrv.2018.03.005] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/03/2017] [Revised: 03/26/2018] [Accepted: 03/27/2018] [Indexed: 02/01/2023]
Abstract
Outdoor air pollution is increasingly identified as a contributor to respiratory and cardiovascular disease. Pro-inflammatory particles and gases are inhaled deep into the lungs, and are associated with impaired lung growth and exacerbations of chronic respiratory diseases. The magnitude of these effects are of interest to patients and families, and have been assessed in studies specific to CF. Using systematic review methodology, we sought to collate these studies in order to summarise the known effects of air pollution in cystic fibrosis, and to present information on decreasing personal air pollution exposures.
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Affiliation(s)
- Rossa Brugha
- Gene Therapy, National Heart and Lung Institute, Imperial College London, Emmanuel Kaye Building, Manresa Road, London SW3 6LR, United Kingdom.
| | - Claire Edmondson
- Gene Therapy, National Heart and Lung Institute, Imperial College London, Emmanuel Kaye Building, Manresa Road, London SW3 6LR, United Kingdom.
| | - Jane C Davies
- Gene Therapy, National Heart and Lung Institute, Imperial College London, Emmanuel Kaye Building, Manresa Road, London SW3 6LR, United Kingdom.
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Effects of Fine Particulate Matter on Pseudomonas aeruginosa Adhesion and Biofilm Formation In Vitro. BIOMED RESEARCH INTERNATIONAL 2018; 2018:6287932. [PMID: 30069474 PMCID: PMC6057421 DOI: 10.1155/2018/6287932] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 03/08/2018] [Revised: 05/09/2018] [Accepted: 05/31/2018] [Indexed: 11/21/2022]
Abstract
Respiratory infections of Pseudomonas aeruginosa are a major cause of mortality and morbidity for hospitalized patients. Fine particulate matter (FPM) is known to have interactions with some bacterial infection in the respiratory system. In this report, we investigate the effect of different concentration of FPM on P. aeruginosa attachment and biofilm formation using in vitro cell culture systems. P. aeruginosa were cultured to form mature biofilms on hydroxyapatite-coated peg and the number of bacteria in the biofilms was enumerated. Morphology of biofilm was imaged with scanning electron microscopy and confocal laser scanning microscopy. Bacterial affinity change to the cell membrane was evaluated with attached colony counting and fluorescence microscopy images. Alteration of bacterial surface hydrophobicity and S100A4 protein concentration were explored as mechanisms of P. aeruginosa adhesion to human cells. There were a concentration-dependent increase of thickness and surface roughness of biofilm mass. P. aeruginosa adherence to respiratory epithelial cells was increased after FPM treatment. Bacterial surface hydrophobicity and S1000A4 protein concentration were increased with proportionally the dose of FPM in media. FPM in the airway could enhance both the adhesion of P. aeruginosa to epithelial cells and biofilm formation. Bacterial surface hydrophobicity and human cell plasma membrane injury are associated with binding of P. aeruginosa on airway epithelial cells and biofilm formation.
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Miyashita L, Suri R, Dearing E, Mudway I, Dove RE, Neill DR, Van Zyl-Smit R, Kadioglu A, Grigg J. E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells. Eur Respir J 2018; 51:1701592. [PMID: 29437942 PMCID: PMC7614837 DOI: 10.1183/13993003.01592-2017] [Citation(s) in RCA: 92] [Impact Index Per Article: 13.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/04/2017] [Accepted: 11/20/2017] [Indexed: 12/31/2022]
Abstract
E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells in vitro, and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletion in vitroThere was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells in vitro Vapour-stimulated adhesion in vitro was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection.
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Affiliation(s)
- Lisa Miyashita
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK
| | - Reetika Suri
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK
| | - Emma Dearing
- The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK
| | - Ian Mudway
- MRC-PHE Centre for Environment and Health, King's College London, London, UK
- NIHR Health Protection Research Unit on Health Impacts of Environmental Hazards, King's College London, London, UK
| | - Rosamund E Dove
- NIHR Health Protection Research Unit on Health Impacts of Environmental Hazards, King's College London, London, UK
| | - Daniel R Neill
- The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK
| | - Richard Van Zyl-Smit
- Division of Pulmonology, Dept of Medicine, University of Cape Town and UCT Lung Institute, Cape Town, South Africa
| | - Aras Kadioglu
- The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK
| | - Jonathan Grigg
- Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK
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Chen X, Liu J, Zhou J, Wang J, Chen C, Song Y, Pan J. Urban particulate matter (PM) suppresses airway antibacterial defence. Respir Res 2018; 19:5. [PMID: 29310642 PMCID: PMC5759166 DOI: 10.1186/s12931-017-0700-0] [Citation(s) in RCA: 55] [Impact Index Per Article: 7.9] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/04/2017] [Accepted: 12/13/2017] [Indexed: 05/23/2025] Open
Abstract
Background Epidemiological studies have shown that urban particulate matter (PM) increases the risk of respiratory infection. However, the underlying mechanisms are poorly understood. PM has been postulated to suppress the activation of airway epithelial innate defence in response to infection. Methods The effects of PM on antibacterial defence were studied using an in vitro infection model. The levels of antimicrobial peptides were measured using RT-PCR and ELISA. In addition to performing colony-forming unit counts and flow cytometry, confocal microscopy was performed to directly observe bacterial invasion upon PM exposure. Results We found that PM PM increased bacterial invasion by impairing the induction of β-defensin-2 (hBD-2), but not the other antimicrobial peptides (APMs) secreted by airway epithelium. PM further increases bacteria-induced ROS production, which is accompanied by an accelerated cell senescence and a decrease in bacteria-induced hBD-2 production, and the antioxidant NAC treatment attenuates these effects. The PM exposure further upregulated the expression of IL-8 but downregulated the expression of IL-13 upon infection. Conclusions PM promotes bacterial invasion of airway epithelial cells by attenuating the induction of hBD-2 via an oxidative burst. These findings associate PM with an increased susceptibility to infection. These findings provide insight into the underlying mechanisms regarding the pathogenesis of particulate matter.
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Affiliation(s)
- Xiaoyan Chen
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Jinguo Liu
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Jian Zhou
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Jian Wang
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Cuicui Chen
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China
| | - Yuanlin Song
- Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
| | - Jue Pan
- Department of Infectious Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
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Chang JH, Hsu SC, Bai KJ, Huang SK, Hsu CW. Association of time-serial changes in ambient particulate matters (PMs) with respiratory emergency cases in Taipei's Wenshan District. PLoS One 2017; 12:e0181106. [PMID: 28732014 PMCID: PMC5521777 DOI: 10.1371/journal.pone.0181106] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/04/2017] [Accepted: 06/25/2017] [Indexed: 12/29/2022] Open
Abstract
Ambient air pollution poses a significant risk for a group of common and often debilitating respiratory diseases, but its direct impact on cause-specific respiratory diseases using emergency room visit (ERV) as an indicator remains to be fully explored. In this study, we conducted a time-series study of ambient PM2.5, NO2, SO2 and their association with ERV for asthma, COPD and pneumonia in a four-year time span. Relative risks for ERV as per log increase in the level of ambient pollutants with time lags of up to 10 days were calculated, using a generalized additive model of Poisson regression. Daily 24-h average concentrations of PM2.5 and pollutant gases were obtained from a local Gutting air quality monitoring station. Results showed that the ERVs for pneumonia and asthma were associated with the level of PM2.5. The effects of PM2.5 on the risk of ERV for asthma were found to be significant at lag days 1 and 2 with increasing risk of 4.34% [RR: 1.091; CI: 1.020-1.166 (95%)] and 3.58% [RR: 1.074; CI: 1.007-1.146 (95%)], respectively. The ERV for pneumonia was associated with the level of PM2.5 at lag days 5, 6 and 7, with increasing risk of 1.92% [RR: 1.039; CI: 1.009-1.070 (95%)], 2.03% [RR: 1.041; CI: 1.009-1.075 (95%)], and 1.82% [RR: 1.037; CI: 1.001-1.075 (95%)], respectively. Further, PM2.5, but not NO2 and SO2, posed a significant risk of ERV for asthma during spring at lag days 0, 1 and 2 (17.12%, RR: 1.408, CI: 1.075-1.238; 15.30%, RR: 1.358 CI: 1.158-1.166; 11.94%, RR: 1.165, CI: 1.004-1.121), which was particularly evident for those who were younger than 75 years of age. In contrast, only PM2.5 was a significant risk of ERV for COPD, which was primarily for those who were younger than 75 years of age during summer season at lag days 3, 4 and 5. (26.66%, RR: 1.704, CI: 1.104-2.632; 26.99%; RR: 1.716, CI: 1.151-2.557; 24.09%; RR: 1.619, CI: 1.111-2.360). Collectively, these results suggested significant seasonal variation and differential time lag effects of PM2.5 on ERV for asthma, COPD and pneumonia.
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Affiliation(s)
- Jer-Hwa Chang
- Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
| | - Shih-Chang Hsu
- Emergency Department, Department of Emergency and Critical Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
| | - Kuan-Jen Bai
- Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
| | - Shau-Ku Huang
- National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan, Miaoli County, Taiwan
- Lou-Hu Hospital, Shen-Zhen University, Shen-Zhen, China
- Research Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
- Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
| | - Chin-Wang Hsu
- Emergency Department, Department of Emergency and Critical Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- Department of Emergency Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
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49
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Hussey SJK, Purves J, Allcock N, Fernandes VE, Monks PS, Ketley JM, Andrew PW, Morrissey JA. Air pollution alters Staphylococcus aureus and Streptococcus pneumoniae biofilms, antibiotic tolerance and colonisation. Environ Microbiol 2017; 19:1868-1880. [PMID: 28195384 PMCID: PMC6849702 DOI: 10.1111/1462-2920.13686] [Citation(s) in RCA: 64] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2016] [Revised: 01/24/2017] [Accepted: 01/30/2017] [Indexed: 01/05/2023]
Abstract
Air pollution is the world's largest single environmental health risk (WHO). Particulate matter such as black carbon is one of the main components of air pollution. The effects of particulate matter on human health are well established however the effects on bacteria, organisms central to ecosystems in humans and in the natural environment, are poorly understood. We report here for the first time that black carbon drastically changes the development of bacterial biofilms, key aspects of bacterial colonisation and survival. Our data show that exposure to black carbon induces structural, compositional and functional changes in the biofilms of both S. pneumoniae and S. aureus. Importantly, the tolerance of the biofilms to multiple antibiotics and proteolytic degradation is significantly affected. Additionally, our results show that black carbon impacts bacterial colonisation in vivo. In a mouse nasopharyngeal colonisation model, black carbon caused S. pneumoniae to spread from the nasopharynx to the lungs, which is essential for subsequent infection. Therefore our study highlights that air pollution has a significant effect on bacteria that has been largely overlooked. Consequently these findings have important implications concerning the impact of air pollution on human health and bacterial ecosystems worldwide.
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Affiliation(s)
- Shane. J. K. Hussey
- Department of Genetics, Adrian BuildingUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
| | - Joanne Purves
- Department of Genetics, Adrian BuildingUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
| | - Natalie Allcock
- Centre for Core Biotechnology Services, Adrian BuildingUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
| | - Vitor E. Fernandes
- Department of InfectionImmunity and Inflammation, Medical Sciences Building, University of Leicester, University RoadLeicesterLE1 9HNLeicestershire, UK
| | - Paul S. Monks
- Department of ChemistryUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
| | - Julian M. Ketley
- Department of Genetics, Adrian BuildingUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
| | - Peter W. Andrew
- Department of InfectionImmunity and Inflammation, Medical Sciences Building, University of Leicester, University RoadLeicesterLE1 9HNLeicestershire, UK
| | - Julie A. Morrissey
- Department of Genetics, Adrian BuildingUniversity of Leicester, University RoadLeicesterLE1 7RHLeicestershire, UK
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50
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Kc R, Shukla SD, Walters EH, O'Toole RF. Temporal upregulation of host surface receptors provides a window of opportunity for bacterial adhesion and disease. MICROBIOLOGY-SGM 2017; 163:421-430. [PMID: 28113047 DOI: 10.1099/mic.0.000434] [Citation(s) in RCA: 25] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/18/2022]
Abstract
Host surface receptors provide bacteria with a foothold from which to attach, colonize and, in some cases, invade tissue and elicit human disease. In this review, we discuss several key host receptors and cognate adhesins that function in bacterial pathogenesis. In particular, we examine the elevated expression of host surface receptors such as CEACAM-1, CEACAM-6, ICAM-1 and PAFR in response to specific stimuli. We explore how upregulated receptors, in turn, expose the host to a range of bacterial infections in the respiratory tract. It is apparent that exploitation of receptor induction for bacterial adherence is not unique to one body system, but is also observed in the central nervous, gastrointestinal and urogenital systems. Prokaryotic pathogens which utilize this mechanism for their infectivity include Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis and Escherichia coli. A number of approaches have been used, in both in vitro and in vivo experimental models, to inhibit bacterial attachment to temporally expressed host receptors. Some of these novel strategies may advance future targeted interventions for the prevention and treatment of bacterial disease.
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Affiliation(s)
- Rajendra Kc
- School of Medicine, Faculty of Health, University of Tasmania, Hobart, TAS 7000, Australia
| | - Shakti D Shukla
- School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, The University of Newcastle, Newcastle, NSW 2308, Australia.,Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, New Lambton Heights, Newcastle, NSW 2305, Australia
| | - Eugene H Walters
- School of Medicine, Faculty of Health, University of Tasmania, Hobart, TAS 7000, Australia
| | - Ronan F O'Toole
- School of Medicine, Faculty of Health, University of Tasmania, Hobart, TAS 7000, Australia
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