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Sato S, Iino C, Sasada T, Soma G, Furusawa K, Yoshida K, Sawada K, Mikami T, Nakaji S, Sakuraba H, Fukuda S. Epidemiological Study on the Interaction between the PNPLA3 (rs738409) and Gut Microbiota in Metabolic Dysfunction-Associated Steatotic Liver Disease. Genes (Basel) 2024; 15:1172. [PMID: 39336763 PMCID: PMC11430940 DOI: 10.3390/genes15091172] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/18/2024] [Revised: 08/31/2024] [Accepted: 09/02/2024] [Indexed: 09/30/2024] Open
Abstract
Many factors are associated with the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD); however, genetics and gut microbiota are representative factors. Recent studies have highlighted the link between host genes and the gut microbiota. Although there have been many studies on the separate effects of single nucleotide polymorphisms (SNPs) and gut bacteria on MASLD, few epidemiological studies have examined how SNPs and gut bacteria interact in the development and progression of MASLD. This study aimed to investigate the association between PNPLA3 rs738409, a representative MASLD-related SNP, and gut bacteria in MASLD using a cross-sectional study of the general population. The 526 participants (318 normal and 208 MASLD groups) were grouped into the PNPLA3 rs738409 SNP, CC, CG, and GG genotypes, and the differences in the gut microbiota were investigated in each group. The PNPLA3 rs738409 CC and CG genotypes were associated with decreased Blautia and Ruminococcaceae in the MASLD group. They were negatively correlated with controlled attenuation parameter levels, body mass index, serum blood glucose, and triglycerides. In contrast, there was no association between the normal and MASLD groups and the gut bacteria in the PNPLA3 rs738409, the GG genotype group. This finding implies that dietary interventions and probiotics may be more effective in preventing and treating MASLD in individuals with the PNPLA3 rs738409 CC and CG genotypes. In contrast, their efficacy may be limited in those with the GG genotype.
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Affiliation(s)
- Satoshi Sato
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Chikara Iino
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Takafumi Sasada
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Go Soma
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Keisuke Furusawa
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Kenta Yoshida
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Kaori Sawada
- Department of Preemptive Medicine, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Tatsuya Mikami
- Department of Preemptive Medicine, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Shigeyuki Nakaji
- Department of Preemptive Medicine, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Hirotake Sakuraba
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
| | - Shinsaku Fukuda
- Department of Gastroenterology, Hematology, and Clinical Immunology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan
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Midori Y, Nosaka T, Hiramatsu K, Akazawa Y, Tanaka T, Takahashi K, Naito T, Matsuda H, Ohtani M, Nakamoto Y. Isolation of mucosa-associated microbiota dysbiosis in the ascending colon in hepatitis C virus post-sustained virologic response cirrhotic patients. Front Cell Infect Microbiol 2024; 14:1371429. [PMID: 38650735 PMCID: PMC11033736 DOI: 10.3389/fcimb.2024.1371429] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2024] [Accepted: 03/25/2024] [Indexed: 04/25/2024] Open
Abstract
Background Achieving sustained virologic response (SVR) in patients infected with hepatitis C virus (HCV) reduces all-cause mortality. However, the mechanisms and risk factors for liver fibrosis and portal hypertension post-SVR remain incompletely understood. In the gut-liver axis, mucosa-associated microbiota (MAM) substantially influence immune and metabolic functions, displaying spatial heterogeneity at the anatomical intestinal site. We analyzed MAM composition and function to isolate the locoregional MAM involved in chronic liver disease progression in HCV post-SVR patients. Methods We collected MAM samples from three intestinal sites (terminal ileum, ascending colon, and sigmoid colon) via brushing during colonoscopy in 23 HCV post-SVR patients and 25 individuals without liver disease (controls). The 16S rRNA of bacterial DNA in specimens collected with a brush and in feces was sequenced. The molecular expression of intestinal tissues and hepatic tissues were evaluated by quantitative real-time PCR. Results In the post-SVR group, the microbial β-diversity of MAM, especially in the ascending colon, differed from the control group and was associated with liver fibrosis progression. In PICRUSt analysis, MAM in the ascending colon in the liver cirrhosis (LC) group showed compromised functions associated with the intestinal barrier and bile acid production, and FGF19 expression was markedly decreased in the terminal ileum biopsy tissue in the LC group. At the genus level, six short-chain fatty acid (SCFA)-producing bacterial genera, Blautia, Alistipes, Roseburia, Agathobaculum, Dorea, and Pseudoflavonifractor were reduced in the ascending colon of post-SVR LC patients. Conclusion In patients of HCV post-SVR, we identified the association between the degree of liver fibrosis and dysbiosis of mucosa-associated SCFA-producing bacterial genera that may be related to intestinal barrier and bile acid production in the ascending colon.
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Affiliation(s)
- Yohei Midori
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Takuto Nosaka
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Katsushi Hiramatsu
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
- Department of General Internal Medicine, Fukui-ken Saiseikai Hospital, Fukui, Japan
| | - Yu Akazawa
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Tomoko Tanaka
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Kazuto Takahashi
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Tatsushi Naito
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Hidetaka Matsuda
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Masahiro Ohtani
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
| | - Yasunari Nakamoto
- Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan
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Nie G, Zhang H, Xie D, Yan J, Li X. Liver cirrhosis and complications from the perspective of dysbiosis. Front Med (Lausanne) 2024; 10:1320015. [PMID: 38293307 PMCID: PMC10824916 DOI: 10.3389/fmed.2023.1320015] [Citation(s) in RCA: 3] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/11/2023] [Accepted: 12/26/2023] [Indexed: 02/01/2024] Open
Abstract
The gut-liver axis refers to the intimate relationship and rigorous interaction between the gut and the liver. The intestinal barrier's integrity is critical for maintaining liver homeostasis. The liver operates as a second firewall in this interaction, limiting the movement of potentially dangerous compounds from the gut and, as a result, contributing in barrier management. An increasing amount of evidence shows that increased intestinal permeability and subsequent bacterial translocation play a role in liver damage development. The major pathogenic causes in cirrhotic individuals include poor intestinal permeability, nutrition, and intestinal flora dysbiosis. Portal hypertension promotes intestinal permeability and bacterial translocation in advanced liver disease, increasing liver damage. Bacterial dysbiosis is closely related to the development of cirrhosis and its related complications. This article describes the potential mechanisms of dysbiosis in liver cirrhosis and related complications, such as spontaneous bacterial peritonitis, hepatorenal syndrome, portal vein thrombosis, hepatic encephalopathy, and hepatocellular carcinoma, using dysbiosis of the intestinal flora as an entry point.
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Affiliation(s)
- Guole Nie
- The First School of Clinical Medicine, Lanzhou University, Lanzhou, China
| | - Honglong Zhang
- The First School of Clinical Medicine, Lanzhou University, Lanzhou, China
| | - Danna Xie
- The First School of Clinical Medicine, Lanzhou University, Lanzhou, China
| | - Jun Yan
- The First School of Clinical Medicine, Lanzhou University, Lanzhou, China
- Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou, China
- Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province, Lanzhou, China
- Cancer Prevention and Control Center of Lanzhou University Medical School, Lanzhou, China
- Gansu Institute of Hepatobiliary and Pancreatic Surgery, Lanzhou, China
- Gansu Clinical Medical Research Center of General Surgery, Lanzhou, China
| | - Xun Li
- The First School of Clinical Medicine, Lanzhou University, Lanzhou, China
- Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou, China
- Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province, Lanzhou, China
- Cancer Prevention and Control Center of Lanzhou University Medical School, Lanzhou, China
- Gansu Institute of Hepatobiliary and Pancreatic Surgery, Lanzhou, China
- Gansu Clinical Medical Research Center of General Surgery, Lanzhou, China
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Kouroumalis E, Tsomidis I, Voumvouraki A. Viral Liver Disease and Intestinal Gut–Liver Axis. GASTROINTESTINAL DISORDERS 2024; 6:64-93. [DOI: 10.3390/gidisord6010005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/03/2025] Open
Abstract
The intestinal microbiota is closely related to liver diseases via the intestinal barrier and bile secretion to the gut. Impairment of the barrier can translocate microbes or their components to the liver where they can contribute to liver damage and fibrosis. The components of the barrier are discussed in this review along with the other elements of the so-called gut–liver axis. This bidirectional relation has been widely studied in alcoholic and non-alcoholic liver disease. However, the involvement of microbiota in the pathogenesis and treatment of viral liver diseases have not been extensively studied, and controversial data have been published. Therefore, we reviewed data regarding the integrity and function of the intestinal barrier and the changes of the intestinal microbioma that contribute to progression of Hepatitis B (HBV) and Hepatitis C (HCV) infection. Their consequences, such as cirrhosis and hepatic encephalopathy, were also discussed in connection with therapeutic interventions such as the effects of antiviral eradication and the use of probiotics that may influence the outcome of liver disease. Profound alterations of the microbioma with significant reduction in microbial diversity and changes in the abundance of both beneficial and pathogenic bacteria were found.
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Affiliation(s)
- Elias Kouroumalis
- Department of Gastroenterology, Medical School, University of Crete, 71500 Heraklion, Greece
| | - Ioannis Tsomidis
- Department of Gastroenterology, Medical School, University of Crete, 71500 Heraklion, Greece
| | - Argyro Voumvouraki
- 1st Department of Internal Medicine, AHEPA University Hospital, 54621 Thessaloniki, Greece
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Mo Z, Wang J, Meng X, Li A, Li Z, Que W, Wang T, Tarnue KF, Ma X, Liu Y, Yan S, Wu L, Zhang R, Pei J, Wang X. The Dose-Response Effect of Fluoride Exposure on the Gut Microbiome and Its Functional Pathways in Rats. Metabolites 2023; 13:1159. [PMID: 37999254 PMCID: PMC10672837 DOI: 10.3390/metabo13111159] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2023] [Revised: 11/13/2023] [Accepted: 11/14/2023] [Indexed: 11/25/2023] Open
Abstract
Metabolic activities within the gut microbiome are intimately linked to human health and disease, especially within the context of environmental exposure and its potential ramifications. Perturbations within this microbiome, termed "gut microbiome perturbations", have emerged as plausible intermediaries in the onset or exacerbation of diseases following environmental chemical exposures, with fluoride being a compound of particular concern. Despite the well-documented adverse impacts of excessive fluoride on various human physiological systems-ranging from skeletal to neurological-the nuanced dynamics between fluoride exposure, the gut microbiome, and the resulting dose-response relationship remains a scientific enigma. Leveraging the precision of 16S rRNA high-throughput sequencing, this study meticulously examines the ramifications of diverse fluoride concentrations on the gut microbiome's composition and functional capabilities within Wistar rats. Our findings indicate a profound shift in the intestinal microbial composition following fluoride exposure, marked by a dose-dependent modulation in the abundance of key genera, including Pelagibacterium, Bilophila, Turicibacter, and Roseburia. Moreover, discernible alterations were observed in critical functional and metabolic pathways of the microbiome, such as D-lyxose ketol-isomerase and DNA polymerase III subunit gamma/tau, underscoring the broad-reaching implications of fluoride exposure. Intriguingly, correlation analyses elucidated strong associations between specific bacterial co-abundance groups (CAGs) and these shifted metabolic pathways. In essence, fluoride exposure not only perturbs the compositional equilibrium of the gut microbiota but also instigates profound shifts in its metabolic landscape. These intricate alterations may provide a mechanistic foundation for understanding fluoride's potential toxicological effects mediated via gut microbiome modulation.
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Affiliation(s)
- Zhe Mo
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
- Department of Environmental Health, Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou 310051, China
| | - Jian Wang
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Xinyue Meng
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Ailin Li
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Zhe Li
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Wenjun Que
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Tuo Wang
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Korto Fatti Tarnue
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Xu Ma
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Ying Liu
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Shirui Yan
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Lei Wu
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Rui Zhang
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Junrui Pei
- Key Laboratory of Etiology and Epidemiology, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control, Education Bureau of Heilongjiang Province & National Health Commission (23618504), Institute for Fluorosis Disease Control, Harbin Medical University, Harbin 150081, China; (Z.M.); (J.W.); (X.M.); (A.L.); (Z.L.); (W.Q.); (T.W.); (K.F.T.); (X.M.); (Y.L.); (S.Y.); (L.W.); (R.Z.)
| | - Xiaofeng Wang
- Department of Environmental Health, Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou 310051, China
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Xiang Z, Wu J, Li J, Zheng S, Wei X, Xu X. Gut Microbiota Modulation: A Viable Strategy to Address Medical Needs in Hepatocellular Carcinoma and Liver Transplantation. ENGINEERING 2023; 29:59-72. [DOI: 10.1016/j.eng.2022.12.012] [Citation(s) in RCA: 17] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/05/2024]
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Stojic J, Kukla M, Grgurevic I. The Intestinal Microbiota in the Development of Chronic Liver Disease: Current Status. Diagnostics (Basel) 2023; 13:2960. [PMID: 37761327 PMCID: PMC10528663 DOI: 10.3390/diagnostics13182960] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2023] [Revised: 09/06/2023] [Accepted: 09/11/2023] [Indexed: 09/29/2023] Open
Abstract
Chronic liver disease (CLD) is a significant global health burden, leading to millions of deaths annually. The gut-liver axis plays a pivotal role in this context, allowing the transport of gut-derived products directly to the liver, as well as biological compounds from the liver to the intestine. The gut microbiota plays a significant role in maintaining the health of the digestive system. A change in gut microbiome composition as seen in dysbiosis is associated with immune dysregulation, altered energy and gut hormone regulation, and increased intestinal permeability, contributing to inflammatory mechanisms and damage to the liver, irrespective of the underlying etiology of CLD. The aim of this review is to present the current knowledge about the composition of the intestinal microbiome in healthy individuals and those with CLD, including the factors that affect this composition, the impact of the altered microbiome on the liver, and the mechanisms by which it occurs. Furthermore, this review analyzes the effects of gut microbiome modulation on the course of CLD, by using pharmacotherapy, nutrition, fecal microbiota transplantation, supplements, and probiotics. This review opens avenues for the translation of knowledge about gut-liver interplay into clinical practice as an additional tool to fight CLD and its complications.
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Affiliation(s)
- Josip Stojic
- Department of Gastroenterology, Hepatology and Clinical Nutrition, University Hospital Dubrava, 10000 Zagreb, Croatia;
| | - Michał Kukla
- Department of Internal Medicine and Geriatrics, Faculty of Medicine, Jagellonian University Medical College, 31-688 Kraków, Poland;
- Department of Endoscopy, University Hospital, 30-688 Kraków, Poland
| | - Ivica Grgurevic
- Department of Gastroenterology, Hepatology and Clinical Nutrition, University Hospital Dubrava, 10000 Zagreb, Croatia;
- School of Medicine, University of Zagreb, 10000 Zagreb, Croatia
- Faculty of Pharmacy and Biochemistry, University of Zagreb, 10000 Zagreb, Croatia
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Yang X, Mai H, Zhou J, Li Z, Wang Q, Lan L, Lu F, Yang X, Guo B, Ye L, Cui P, Liang H, Huang J. Alterations of the gut microbiota associated with the occurrence and progression of viral hepatitis. Front Cell Infect Microbiol 2023; 13:1119875. [PMID: 37342245 PMCID: PMC10277638 DOI: 10.3389/fcimb.2023.1119875] [Citation(s) in RCA: 7] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/09/2022] [Accepted: 05/22/2023] [Indexed: 06/22/2023] Open
Abstract
Background Gut microbiota is the largest population of microorganisms and is closely related to health. Many studies have explored changes in gut microbiota in viral hepatitis. However, the correlation between gut microbiota and the occurrence and progression of viral hepatitis has not been fully clarified. Methods PubMed and BioProject databases were searched for studies about viral hepatitis disease and 16S rRNA gene sequencing of gut microbiota up to January 2023. With bioinformatics analyses, we explored changes in microbial diversity of viral hepatitis, screened out crucial bacteria and microbial functions related to viral hepatitis, and identified the potential microbial markers for predicting risks for the occurrence and progression of viral hepatitis based on ROC analysis. Results Of the 1389 records identified, 13 studies met the inclusion criteria, with 950 individuals including 656 patient samples (HBV, n = 546; HCV, n = 86; HEV, n = 24) and 294 healthy controls. Gut microbial diversity is significantly decreased as the infection and progression of viral hepatitis. Alpha diversity and microbiota including Butyricimonas, Escherichia-Shigella, Lactobacillus, and Veillonella were identified as the potential microbial markers for predicting the risk of development of viral hepatitis (AUC>0.7). Microbial functions including tryptophan metabolism, fatty acid biosynthesis, lipopolysaccharide biosynthesis, and lipid metabolism related to the microbial community increased significantly as the development of viral hepatitis. Conclusions This study demonstrated comprehensively the gut microbiota characteristics in viral hepatitis, screened out crucial microbial functions related to viral hepatitis, and identified the potential microbial markers for predicting the risk of viral hepatitis.
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Affiliation(s)
- Xing Yang
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Huanzhuo Mai
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Jie Zhou
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Zhuoxin Li
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Qing Wang
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Liuyan Lan
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Fang Lu
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Xiping Yang
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Baodong Guo
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Li Ye
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
| | - Ping Cui
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
- Life Science Institute, Guangxi Medical University, Nanning, China
- Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning, China
| | - Hao Liang
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
- Life Science Institute, Guangxi Medical University, Nanning, China
- Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning, China
| | - Jiegang Huang
- School of Public Health, Guangxi Medical University, Nanning, China
- Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Universities Key Laboratory of Prevention and Control of Highly Prevalent Disease, Guangxi Medical University, Nanning, China
- Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, Guangxi Medical University, Nanning, China
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9
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El-Mowafy M, Elegezy M, El-Mesery M, Elgaml A. Novel method for cloning of hepatitis B virus DNA using the In-Fusion enzyme. GENE REPORTS 2023. [DOI: 10.1016/j.genrep.2023.101765] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/28/2023]
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10
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Maciel-Fiuza MF, Muller GC, Campos DMS, do Socorro Silva Costa P, Peruzzo J, Bonamigo RR, Veit T, Vianna FSL. Role of gut microbiota in infectious and inflammatory diseases. Front Microbiol 2023; 14:1098386. [PMID: 37051522 PMCID: PMC10083300 DOI: 10.3389/fmicb.2023.1098386] [Citation(s) in RCA: 66] [Impact Index Per Article: 33.0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2022] [Accepted: 03/06/2023] [Indexed: 03/29/2023] Open
Abstract
Thousands of microorganisms compose the human gut microbiota, fighting pathogens in infectious diseases and inhibiting or inducing inflammation in different immunological contexts. The gut microbiome is a dynamic and complex ecosystem that helps in the proliferation, growth, and differentiation of epithelial and immune cells to maintain intestinal homeostasis. Disorders that cause alteration of this microbiota lead to an imbalance in the host’s immune regulation. Growing evidence supports that the gut microbial community is associated with the development and progression of different infectious and inflammatory diseases. Therefore, understanding the interaction between intestinal microbiota and the modulation of the host’s immune system is fundamental to understanding the mechanisms involved in different pathologies, as well as for the search of new treatments. Here we review the main gut bacteria capable of impacting the immune response in different pathologies and we discuss the mechanisms by which this interaction between the immune system and the microbiota can alter disease outcomes.
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Affiliation(s)
- Miriãn Ferrão Maciel-Fiuza
- Postgraduate Program in Genetics and Molecular Biology, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Instituto Nacional de Genética Médica Populacional, Porto Alegre, Brazil
- Genomics Medicine Laboratory, Center of Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
- Laboratory of Immunobiology and Immunogenetics, Department of Genetics, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
| | - Guilherme Cerutti Muller
- Postgraduate Program in Genetics and Molecular Biology, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
| | - Daniel Marques Stuart Campos
- Genomics Medicine Laboratory, Center of Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
- Laboratory of Immunobiology and Immunogenetics, Department of Genetics, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
| | - Perpétua do Socorro Silva Costa
- Postgraduate Program in Genetics and Molecular Biology, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Instituto Nacional de Genética Médica Populacional, Porto Alegre, Brazil
- Department of Nursing, Universidade Federal do Maranhão, Imperatriz, Brazil
| | - Juliano Peruzzo
- Dermatology Service of Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
- Postgraduate Program in Medicine, Medical Sciences, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
| | - Renan Rangel Bonamigo
- Dermatology Service of Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
- Postgraduate Program in Medicine, Medical Sciences, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Postgraduate Program in Pathology, Universidade Federal De Ciências Da Saúde de Porto Alegre, Porto Alegre, Brazil
| | - Tiago Veit
- Laboratory of Immunobiology and Immunogenetics, Department of Genetics, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Department of Microbiology, Immunology and Parasitology, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil
| | - Fernanda Sales Luiz Vianna
- Postgraduate Program in Genetics and Molecular Biology, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Instituto Nacional de Genética Médica Populacional, Porto Alegre, Brazil
- Genomics Medicine Laboratory, Center of Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
- Laboratory of Immunobiology and Immunogenetics, Department of Genetics, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- Postgraduate Program in Medicine, Medical Sciences, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil
- *Correspondence: Fernanda Sales Luiz Vianna,
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11
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Marascio N, De Caro C, Quirino A, Mazzitelli M, Russo E, Torti C, Matera G. The Role of the Microbiota Gut-Liver Axis during HCV Chronic Infection: A Schematic Overview. J Clin Med 2022; 11:5936. [PMID: 36233804 PMCID: PMC9572099 DOI: 10.3390/jcm11195936] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2022] [Revised: 10/03/2022] [Accepted: 10/04/2022] [Indexed: 11/30/2022] Open
Abstract
Hepatitis C virus (HCV) still represents one of the most important worldwide health care problems. Since 2011, direct-acting antiviral (DAA) drugs have increased the number of people who have achieved a sustained virological response (SVR). Even if the program to eradicate HCV by 2030 is still ongoing, the SARS-CoV-2 pandemic has created a delay due to the reallocation of public health resources. HCV is characterized by high genetic variability and is responsible for hepatic and extra-hepatic diseases. Depending on the HCV genotype/subtype and comorbidities of patients, tailored treatment is necessary. Recently, it has been shown that liver damage impacts gut microbiota, altering the microbial community (dysbiosis) during persistent viral replication. An increasing number of studies are trying to clarify the role of the gut-liver axis during HCV chronic infection. DAA therapy, by restoring the gut microbiota equilibrium, seems to improve liver disease progression in both naïve and treated HCV-positive patients. In this review, we aim to discuss a snapshot of selected peer-reviewed papers concerning the interplay between HCV and the gut-liver axis.
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Affiliation(s)
- Nadia Marascio
- Clinical Microbiology Unit, Department of Health Science, “Magna Graecia” University, 88100 Catanzaro, Italy
| | - Carmen De Caro
- System and Applied Pharmacology, Department of Health Science, “Magna Graecia” University, 88100 Catanzaro, Italy
| | - Angela Quirino
- Clinical Microbiology Unit, Department of Health Science, “Magna Graecia” University, 88100 Catanzaro, Italy
| | - Maria Mazzitelli
- Infectious and Tropical Diseases Unit, University Hospital of Padua, 35128 Padua, Italy
| | - Emilio Russo
- System and Applied Pharmacology, Department of Health Science, “Magna Graecia” University, 88100 Catanzaro, Italy
| | - Carlo Torti
- Infectious and Tropical Diseases Unit, Department of Medical and Surgical Sciences, “Magna Graecia” University, 88100 Catanzaro, Italy
| | - Giovanni Matera
- Clinical Microbiology Unit, Department of Health Science, “Magna Graecia” University, 88100 Catanzaro, Italy
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12
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Hartmann P. Editorial: The Microbiome in Hepatobiliary and Intestinal Disease. Front Physiol 2022; 13:893074. [PMID: 35492588 PMCID: PMC9044070 DOI: 10.3389/fphys.2022.893074] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/09/2022] [Accepted: 03/11/2022] [Indexed: 12/12/2022] Open
Affiliation(s)
- Phillipp Hartmann
- Department of Pediatrics, University of California, San Diego, San Diego, CA, United States
- Division of Gastroenterology, Hepatology and Nutrition, Rady Children’s Hospital San Diego, San Diego, CA, United States
- *Correspondence: Phillipp Hartmann,
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13
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Compositions of gut microbiota before and shortly after hepatitis C viral eradication by direct antiviral agents. Sci Rep 2022; 12:5481. [PMID: 35361930 PMCID: PMC8971444 DOI: 10.1038/s41598-022-09534-w] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/23/2021] [Accepted: 03/08/2022] [Indexed: 12/24/2022] Open
Abstract
It is unclear whether dysbiosis in hepatitis C virus (HCV) infected patients results from the viral infection per se or develops as a result of hepatic dysfunction. We aimed to characterize compositions in gut microbiome before and shortly after HCV clearance. In this prospective cohort study, adult patients with confirmed HCV viremia were screened before receiving direct antiviral agents. Those with recent exposure to antibiotics or probiotics (within one month), prior abdominal surgery, or any malignancy were ineligible. Stool was collected before antiviral therapy started and at 12 weeks after the treatment completed. From the extracted bacterial DNA, 16 s rRNA gene was amplified and sequenced. Each patient was matched 1:2 in age and sex with uninfected controls. A total of 126 individuals were enrolled into analysis. The gut microbiome was significantly different between HCV-infected patients (n = 42), with or without cirrhosis, and their age-and sex-matched controls (n = 84) from the levels of phylum to amplicon sequence variant (all p values < 0.01 by principal coordinates analysis). All patients achieved viral eradication and exhibited no significant changes in the overall composition of gut microbiome following viral eradication (all p values > 0.5), also without significant difference in alpha diversity (all p values > 0.5). For the purpose of exploration, we also reported bacteria found differently abundant before and after HCV eradication, including Coriobacteriaceae, Peptostreptococcaceae, Staphylococcaceae, Morganellaceae, Pasteurellaceae, Succinivibrionaceae, and Moraxellaceae. Gut microbiota is altered in HCV-infected patients as compared with uninfected controls, but the overall microbial compositions do not significantly change shortly after HCV eradication.
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14
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Gut Microbiota Extracellular Vesicles as Signaling Molecules Mediating Host-Microbiota Communications. Int J Mol Sci 2021; 22:ijms222313166. [PMID: 34884969 PMCID: PMC8658398 DOI: 10.3390/ijms222313166] [Citation(s) in RCA: 30] [Impact Index Per Article: 7.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/15/2021] [Revised: 11/30/2021] [Accepted: 11/30/2021] [Indexed: 12/15/2022] Open
Abstract
Over the past decade, gut microbiota dysbiosis has been linked to many health disorders; however, the detailed mechanism of this correlation remains unclear. Gut microbiota can communicate with the host through immunological or metabolic signalling. Recently, microbiota-released extracellular vesicles (MEVs) have emerged as significant mediators in the intercellular signalling mechanism that could be an integral part of microbiota-host communications. MEVs are small membrane-bound vesicles that encase a broad spectrum of biologically active compounds (i.e., proteins, mRNA, miRNA, DNA, carbohydrates, and lipids), thus mediating the horizontal transfer of their cargo across intra- and intercellular space. In this study, we provide a comprehensive and in-depth discussion of the biogenesis of microbial-derived EVs, their classification and routes of production, as well as their role in inter-bacterial and inter-kingdom signaling.
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15
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Sultan S, El-Mowafy M, Elgaml A, Ahmed TAE, Hassan H, Mottawea W. Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease. Front Physiol 2021; 12:715506. [PMID: 34646151 PMCID: PMC8502967 DOI: 10.3389/fphys.2021.715506] [Citation(s) in RCA: 71] [Impact Index Per Article: 17.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2021] [Accepted: 08/18/2021] [Indexed: 12/12/2022] Open
Abstract
Inflammatory bowel diseases (IBD) are chronic medical disorders characterized by recurrent gastrointestinal inflammation. While the etiology of IBD is still unknown, the pathogenesis of the disease results from perturbations in both gut microbiota and the host immune system. Gut microbiota dysbiosis in IBD is characterized by depleted diversity, reduced abundance of short chain fatty acids (SCFAs) producers and enriched proinflammatory microbes such as adherent/invasive E. coli and H2S producers. This dysbiosis may contribute to the inflammation through affecting either the immune system or a metabolic pathway. The immune responses to gut microbiota in IBD are extensively discussed. In this review, we highlight the main metabolic pathways that regulate the host-microbiota interaction. We also discuss the reported findings indicating that the microbial dysbiosis during IBD has a potential metabolic impact on colonocytes and this may underlie the disease progression. Moreover, we present the host metabolic defectiveness that adds to the impact of symbiont dysbiosis on the disease progression. This will raise the possibility that gut microbiota dysbiosis associated with IBD results in functional perturbations of host-microbiota interactions, and consequently modulates the disease development. Finally, we shed light on the possible therapeutic approaches of IBD through targeting gut microbiome.
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Affiliation(s)
- Salma Sultan
- Faculty of Health Sciences, School of Nutrition Sciences, University of Ottawa, Ottawa, ON, Canada
| | - Mohammed El-Mowafy
- Department of Microbiology and Immunology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt
| | - Abdelaziz Elgaml
- Department of Microbiology and Immunology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.,Department of Microbiology and Immunology, Faculty of Pharmacy, Horus University, New Damietta, Egypt
| | - Tamer A E Ahmed
- Faculty of Health Sciences, School of Nutrition Sciences, University of Ottawa, Ottawa, ON, Canada.,Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada
| | - Hebatoallah Hassan
- Faculty of Health Sciences, School of Nutrition Sciences, University of Ottawa, Ottawa, ON, Canada.,Department of Biotechnology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt
| | - Walid Mottawea
- Faculty of Health Sciences, School of Nutrition Sciences, University of Ottawa, Ottawa, ON, Canada.,Department of Microbiology and Immunology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt
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16
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Milosevic I, Russo E, Vujovic A, Barac A, Stevanovic O, Gitto S, Amedei A. Microbiota and viral hepatitis: State of the art of a complex matter. World J Gastroenterol 2021; 27:5488-5501. [PMID: 34588747 PMCID: PMC8433613 DOI: 10.3748/wjg.v27.i33.5488] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/02/2021] [Revised: 03/26/2021] [Accepted: 07/21/2021] [Indexed: 02/06/2023] Open
Abstract
Changes in gut microbiota influence both the gut and liver, which are strictly connected by the so-called "gut-liver axis". The gut microbiota acts as a major determinant of this relationship in the onset and clinical course of liver diseases. According to the results of several studies, gut dysbiosis is linked to viral hepatitis, mainly hepatitis C virus and hepatitis B virus infection. Gut bacteria-derived metabolites and cellular components are key molecules that affect liver function and modulate the pathology of viral hepatitis. Recent studies showed that the gut microbiota produces various molecules, such as peptidoglycans, lipopolysaccharides, DNA, lipoteichoic acid, indole-derivatives, bile acids, and trimethylamine, which are translocated to the liver and interact with liver immune cells causing pathological effects. Therefore, the existence of crosstalk between the gut microbiota and the liver and its implications on host health and pathologic status are essential factors impacting the etiology and therapeutic approach. Concrete mechanisms behind the pathogenic role of gut-derived components on the pathogenesis of viral hepatitis remain unclear and not understood. In this review, we discuss the current findings of research on the bidirectional relationship of the components of gut microbiota and the progression of liver diseases and viral hepatitis and vice versa. Moreover, this paper highlights the current therapeutic and preventive strategies, such as fecal transplantation, used to restore the gut microbiota composition and so improve host health.
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Affiliation(s)
- Ivana Milosevic
- Clinic for Infectious and Tropical Diseases, Clinical Centre of Serbia Faculty of Medicine, University of Belgrade, Belgrade 101801, Serbia
| | - Edda Russo
- Department of Experimental and Clinical Medicine, University of Florence, Firenze 50100, Italy
| | - Ankica Vujovic
- Clinic for Infectious and Tropical Diseases, Clinical Centre of Serbia Faculty of Medicine, University of Belgrade, Belgrade 101801, Serbia
| | - Aleksandra Barac
- Clinic for Infectious and Tropical Diseases, Clinical Centre of Serbia Faculty of Medicine, University of Belgrade, Belgrade 101801, Serbia
| | - Olja Stevanovic
- Clinic for Infectious and Tropical Diseases, Clinical Centre of Serbia Faculty of Medicine, University of Belgrade, Belgrade 101801, Serbia
| | - Stefano Gitto
- Department of Experimental and Clinical Medicine, University of Florence, Firenze 50100, Italy
| | - Amedeo Amedei
- Department of Experimental and Clinical Medicine, University of Florence, Firenze 50100, Italy
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17
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Fecal Microbiota Transplantation in Patients with HBV Infection or Other Chronic Liver Diseases: Update on Current Knowledge and Future Perspectives. J Clin Med 2021; 10:jcm10122605. [PMID: 34204748 PMCID: PMC8231596 DOI: 10.3390/jcm10122605] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/14/2021] [Revised: 06/09/2021] [Accepted: 06/10/2021] [Indexed: 12/12/2022] Open
Abstract
Liver disease and gut dysbiosis are strictly associated, and the pathophysiology of this bidirectional relationship has recently been the subject of several investigations. Growing evidence highlights the link between gut microbiota composition, impairment of the gut-liver axis, and the development or progression of liver disease. Therefore, the modulation of gut microbiota to maintain homeostasis of the gut-liver axis could represent a potential instrument to halt liver damage, modify the course of liver disease, and improve clinical outcomes. Among all the methods available to achieve this purpose, fecal microbiota transplantation (FMT) is one of the most promising, being able to directly reshape the recipient’s gut microbial communities. In this review, we report the main characteristics of gut dysbiosis and its pathogenetic consequences in cirrhotic patients, discussing the emerging data on the application of FMT for liver disease in different clinical settings.
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18
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Changes of Gut-Microbiota-Liver Axis in Hepatitis C Virus Infection. BIOLOGY 2021; 10:biology10010055. [PMID: 33451143 PMCID: PMC7828638 DOI: 10.3390/biology10010055] [Citation(s) in RCA: 22] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/12/2020] [Revised: 01/02/2021] [Accepted: 01/08/2021] [Indexed: 12/12/2022]
Abstract
Simple Summary Gut microbiota alteration is linked to many health disorders including hepatitis C virus (HCV) infection. This dysbiosis in turn impacts the coordination between the gut and the liver that is known as the gut–liver-axis. Here, we discuss the latest findings regarding the changes in gut microbiota structure and functionality post HCV infection and its treatment regimens. In addition, we underline the contribution of the microbiota alterations to HCV associated liver complications. Abstract The gut–liver-axis is a bidirectional coordination between the gut, including microbial residents, the gut microbiota, from one side and the liver on the other side. Any disturbance in this crosstalk may lead to a disease status that impacts the functionality of both the gut and the liver. A major cause of liver disorders is hepatitis C virus (HCV) infection that has been illustrated to be associated with gut microbiota dysbiosis at different stages of the disease progression. This dysbiosis may start a cycle of inflammation and metabolic disturbance that impacts the gut and liver health and contributes to the disease progression. This review discusses the latest literature addressing this interplay between the gut microbiota and the liver in HCV infection from both directions. Additionally, we highlight the contribution of gut microbiota to the metabolism of antivirals used in HCV treatment regimens and the impact of these medications on the microbiota composition. This review sheds light on the potential of the gut microbiota manipulation as an alternative therapeutic approach to control the liver complications post HCV infection.
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