Helicobacter pylori (H pylori) infection and H pylori antibodies have been reported to be associated with an increased risk of atrial fibrillation (AF) in several observational studies. However, whether this relationship is causal and which H pylori antibodies serve as the determinant of AF remains largely unclear. Recently published Genome-wide association studies on 7 different antibodies of H pylori-specific proteins and AF (2 correction methods) were included in this study. A two-sample Mendelian randomization study was employed to investigate the causal effects of circulating H pylori antibodies on the risk of AF. Genetically predicted serum H pylori Catalase antibody level was associated with an increased risk of AF (Firth correction) (odds ratio = 1.137, 95% confidence interval: 1.008-1.282, P = .037) and AF (saddlepoint approximation correction) (odds ratio = 1.139, 95% confidence interval: 1.010-1.284, P = .034). No significant causal correlations were found between other H pylori antibodies and AF. This Mendelian randomization study demonstrates that H pylori Catalase antibody is the only causal determinant associated with the risk of AF in terms of H pylori-related antibodies.

The gastrointestinal tract is not only an important component of the digestive system but also a crucial part of the body's immune system. Numerous studies have reported that gastrointestinal immunity plays a critical role in many extraintestinal diseases, including neurodegenerative disorders. However, the relationship between gastric mucosal immunity and neurodegenerative diseases, such as Parkinson's disease(PD), remains underexplored. The rate of H. pylori infection was assessed using the 13 C-Urea Breath Test (13 C-UBT) in a case-control study involving 315 PD patients and a control group of 22,383 outpatients. Multivariate regression and propensity score matching (PSM) analyses were employed to adjust for confounding factors. A lower H. pylori infection rate was found in PD cases compared to outpatient controls (DOB ≥ 8, 22.5% versus 27.5%, p = 0.049; DOB ≥ 4, 28.6% versus 33.9%, p = 0.046). After adjusting for confounding factors, the H. pylori infection rate remained lower in PD cases compared to controls. The study revealed an inverse correlation between H. pylori infection and PD, suggesting that H. pylori infection could potentially act as a protective factor against the development of PD.

The primary aim of this study was to investigate the knowledge, attitude, and practice(KAP) concerning Helicobacter pylori (H. pylori) and the factors influencing them among northeast China individuals. A questionnaire regarding H. pylori, grounded in the KAP theoretical framework, was tailored for northeast China individuals. The questionnaire was conducted online and analyzed statistically. Additionally, structural equation modeling was applied to verify the interconnections among social media usage, knowledge, attitude, and practice. A total of 712 valid questionnaires were analyzed. The mean scores were 2.69 ± 1.03 for knowledge, 4.09 ± 0.81 for attitude, and 3.40 ± 0.73 for practice. Various factors including sex, occupation, and social media usage influenced knowledge, attitude, and practice scores, with social media usage exerting a notable impact on all facets. The structural equation modeling analysis demonstrated that social media usage promoted higher levels of knowledge, attitude, and practice regarding H. pylori. Individuals possessing a higher level of knowledge and attitude concerning H. pylori demonstrated superior preventive practice. Northeast China residents have limited H. pylori knowledge but show a positive attitude and good preventive practice. The utilization of social media has significantly improved the population's knowledge, attitude, and practice concerning H. pylori.

Helicobacter pylori ( H. pylori ) has been inconsistently associated with the risk of Alzheimer disease. The exposure assessment period has often overlapped with the prodromal time of Alzheimer disease. Cognitive disorders might increase vulnerability to infectious pathogens, complicating the ascertainment of the temporal relationship between H. pylori infection and Alzheimer disease.

This Finnish nested case-control study included 70,520 persons with incident Alzheimer disease diagnosed between 2005 and 2011 and 281,233 age-, sex-, and region of residence-matched controls. We obtained information on comorbidities and drug use from the national healthcare registers. We identified dispensed H. pylori eradication treatments from the Prescription Register. We considered exposure at least 5 years before Alzheimer disease diagnosis in the main analysis. We compared the risk of Alzheimer disease between H. pylori eradication treatment users and nonusers using confounder-adjusted (comorbidities and other drug use) conditional logistic regression. We assessed cumulative exposure by calculating the number of eradication treatments.

The prevalence of exposure to H. pylori eradication treatment at least 5 years before the outcome was 4.1% in cases and 3.9% in controls. The odds ratio (95% confidence interval) was 1.06 (1.02, 1.11) in the crude and 1.03 (0.99, 1.07) in the confounder-adjusted model. We observed no association between cumulative exposure and risk of Alzheimer disease.

Our results, reflecting diagnosed and treated H. pylori infection late in life, do not support the hypothesis of H. pylori as an independent risk factor for Alzheimer disease. The previously reported association may be explained by reverse association and confounding.

To explore the possible causal link between stable angina pectoris (SAP) and gastric cancer (GC) through Mendelian randomization analysis. We used data from genome-wide association studies (GWAS) statistical datasets, with SAP and GC screened as relevant instrumental variables for exposure factors, respectively. To evaluate the causal link between SAP and GC, a two-sample bidirectional Mendelian randomization analysis was conducted, leveraging genetic variants as instrumental variables. In addition, effects of horizontal pleiotropy were evaluated using MR-PRESSO and MR-Egger intercept analysis. Sensitivity analysis was performed using Cochran Q test and "leave one out" method. The study showed a significant causal relationship between SAP and GC in the analysis with SAP as the exposure variable (odds ratio [OR] = 0.78, 95% confidence interval [CI] = 0.69-0.87, p = 0.000027 using inverse variance weighting [IVW]). Sensitivity analysis confirmed the robustness of Mendelian randomization results. In the analysis of GC as an exposure variable, gastric cancer and SAP also showed a significant causal association (OR = 0.87, 95%CI = 0.77-0.98, p = 0.024 using IVW), but sensitivity analysis suggested a significant pleiotropy between instrumental variables (p = 0.0093 using MR-Egger intercept analysis), which cast doubt on the reliability of the study and requires careful interpretation of the results. Existing studies suggest that individuals with SAP may have a lower risk of developing GC. However, the precise causal relationship, particularly regarding whether GC contributes to an increased risk of SAP, remains unclear and warrants further investigation. GC and ischemic heart disease which represented by SAP are both associated with oxidative stress in their pathogenesis. Local tissue-induced mitochondrial autophagy or cellular ferroptosis triggers a systemic response, potentially underlying the negative correlation between GC and SAP. Thus, therapeutic strategies that target the interplay between local tissue and systemic responses in oxidative stress may hold promise for the benefits to patients.

Gastric cancer (GC) is one of the most common malignancies worldwide, and Helicobacter pylori (HP) infection is a well-established risk factor for its development. Programmed death-ligand 1 (PD-L1) expression is a crucial biomarker for predicting the efficacy of immune checkpoint inhibitors in cancer treatment. While HP infection and PD-L1 expression in GC may be linked, the relationship between them remains unclear, in part because there have been conflicting results reported from various studies.

To perform a meta-analysis to assess the relationship between HP and PD-L1 expression in patients with GC.

A systematic literature review was conducted using PubMed, Embase, Cochrane Library, and Web of Science databases. Observational studies that examined the association between HP infection and PD-L1 expression in patients with GC were included. Odds ratios and 95% confidence intervals were calculated to estimate the association. Heterogeneity was assessed using Cochrane's Q test and I² statistic. A random-effects model was used due to significant heterogeneity across studies.

Fourteen studies involving a total of 3069 patients with GC were included. The pooled analysis showed a significant association between HP infection and increased PD-L1 expression in GC tissues (odd ratio = 1.69, 95% confidence interval: 1.24-2.29, P < 0.001, I 2 = 59%). Sensitivity analyses confirmed the robustness of these findings. Subgroup analyses did not show significant variation based on geographic region, sample size, or method of PD-L1 assessment. Publication bias was minimal, as shown by funnel plots and Egger's regression test.

HP infection is associated with increased PD-L1 expression in GC, suggesting that HP status may influence the response to programmed cell death protein 1/PD-L1 blockade therapy.

Background/Objectives: Helicobacter pylori is a major risk factor for gastric cancer. The incidence and prevalence of the pathogen are increasing worldwide, urging novel approaches to reduce detection turnaround times. H. pylori diagnosis relies on histological examination of gastric biopsies, but interobserver variability considerably impacts its identification. We present an algorithm combining a feature pyramid network and a ResNet architecture for automatic and rapid H. pylori detection in digitized Warthin-Starry-stained gastric biopsies. Methods: Whole-slide images were segmented into manually annotated smaller patches and segments containing stomach tissue were analyzed for the presence of Gram-negative bacteria. Patches classified as positive were examined to confirm the presence/absence of bacteria in contact with the gastric epithelial surface (H. pylori). Results: The algorithm exhibited 0.923 average precision and 0.982 average recall. The conducted efficiency study demonstrated that algorithm utilization significantly decreased (p < 0.001) diagnostic turnaround times for all participants (two pathologists, a pathology resident, a pathology technician, and a biotechnologist), observing an 88.13-91.76% time reduction. Implementation of the algorithm also improved diagnostic accuracy for the resident, technician, and biotechnologist, indicating that the tool remarkably supports less experienced personnel. Conclusions: We believe that the incorporation of our algorithm into pathology workflows will help standardize diagnostic protocols and drastically reduce H. pylori diagnostic turnaround times.

Inspired by the recognized activity of Ebselen against urease, we optimized the structure of 1,2-benzisoselenazol-3(2H)-one to provide potent inhibitors of ureolysis in Helicobacter pylori cells. To achieve this goal, we combined the elongation of the N-substituent of Ebselen from phenyl to benzyl with halogenation of the aromatic fragment. The modifications implemented provided compounds with activities that were several times better compared to that of the lead compound. In particular, 3-fluoro-4-trifluoromethyl and 2-chloro-5-fluoro derivatives of N-benzyl-1,2-benzisoselenazol-3(2H)-one achieved a remarkable antiureolytic effect in live H. pylori cells (IC50 < 100 nM) that outperformed the data reported so far. This activity was reflected in the antiurease potential measured for the Sporosarcina pasteurii model enzyme, with the highest affinity observed for 2-chloro-5-fluoro and 2,4-dichloro derivatives (K i < 0.6 nM). The best inhibitor demonstrated considerable antibacterial properties on a multidrug-resistant clinical H. pylori isolate in additive combination with clarithromycin (MIC = 0.073 μg/mL).

Activation of inflammasomes is the activation of inflammation‑related caspase mediated by the assembly signal of multi‑protein complex and the maturity of inflammatory factors, such as IL‑1β and IL‑18. Among them, the Nod‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is the most thoroughly studied type of inflammatory corpuscle at present, which is involved in the occurrence and development of numerous human diseases. Therefore, targeting the NLRP3 inflammasome has become the focus of drug development for related diseases. In this paper, the research progress of the NLRP3 inflammasome in recent years is summarized, including the activation and regulation of NLRP3 and its association with diseases. A deep understanding of the regulatory mechanism of NLRP3 will be helpful to the discovery of new drug targets and the development of therapeutic drugs.

Epidemiological and experimental studies have suggested that chronic H. pylori infection may be associated with colorectal cancer (CRC), a topic of growing interest. The Bradford-Hill criteria are the mainstay of the epidemiological approach to causal inference. We aim to evaluate the epidemiological evidence based on the Bradford-Hill causality criteria and the association between H. pylori and CRC.

A literature review of the databases search: Pubmed, ScienceDirect, Embase, SciELO, Cochrane, and Medline. There are no limits in a period. Information sources that were coherent with the objectives set were selected.

Applying the Bradford Hill criteria, we can conclude that H. pylori is positively associated with CRC. The current epidemiological findings should stimulate future studies to explain how H. pylori interacts with intestinal dysbiosis and the role of H. pylori eradication in the treatment and prevention of CRC.

H. pylori reasonably meets the Bradford Hill criteria for causality. Further studies are required to consolidate the data and generate strategies to determine whether H. pylori eradication translates into decreased CRC incidence and mortality in large populations.

The growing global burden of metabolic dysfunction-associated steatohepatitis (MASH) demands a deeper understanding of its underlying mechanisms and risk factors. Recent studies, such as the large population-based case-control analysis by Abdel-Razeq et al, suggest a significant association between Helicobacter pylori (H. pylori) infection and an increased risk of developing MASH. This study provides compelling data supporting this association, even after adjusting for confounders such as obesity, diabetes, and hyperlipidemia. However, the complexity of this relationship remains unresolved, requiring further investigation into the biological, genetic, and environmental pathways that connect these two conditions. This article critically reviews the study's findings and identifies its limitations, offering innovative research directions for the future. Key areas of focus include integrating genomic and microbiome analyses, exploring the impact of H. pylori eradication on MASH progression, studying molecular mechanisms at the intersection of infection and liver disease, and developing personalized therapeutic strategies.

Rheumatoid arthritis (RA) is an autoimmune condition that predominantly affects synovial joints, manifesting with joint swelling, pain, and stiffness. In advanced stages, unchecked inflammation can inflict damage on bone and cartilage, resulting in disabilities and deformities of the joints. Additionally, systemic and extra-articular complications may arise due to the consequences of uncontrolled inflammation. Helicobacter pylori (H. pylori) is one of the most prevalent chronic bacterial infections in humans. This microorganism is a spiral-shaped, flagellated, microaerophilic gram-negative bacterium. Prolonged exposure leads to the activation of the immune system, with infected gastric mucosa epithelial cells continuously producing cytokines. This production, in turn, triggers the generation of antibodies as well as T Helper 1 and T Helper 2 effector T cells. The persistent antigenic stimulation resulting from H. pylori infection could lead to the progression of autoimmune diseases. Numerous clinical and pharmacological trials have illustrated the efficacy of traditional Chinese medicine against H. pylori. This review aims to delve into the connection between H. pylori and rheumatoid arthritis so as understand the pathogenesis. The concluding section of this review explores the interplay of Chinese medicine and Helicobacter pylori concerning rheumatoid arthritis.

One of the most prevalent human infections is Helicobacter pylori (H. pylori), which affects more than half of the global population. Although H. pylori infections are widespread, only a minority of individuals develop severe gastroduodenal disorders. The global resistance of H. pylori to antibiotics has reached concerning levels, significantly impacting the effectiveness of treatment. Consequently, the development of vaccines targeting virulence factors may present a viable alternative for the treatment and prevention of H. pylori infections. This review aims to provide a comprehensive overview of the current understanding of H. pylori infection, with a particular focus on its virulence factors, pathophysiology, and vaccination strategies. This review discusses various virulence factors associated with H. pylori, such as cytotoxin-associated gene A (cagA), vacuolating cytotoxin gene (vacA), outer membrane proteins (OMPs), neutrophil-activated protein (NAP), urease (ure), and catalase. The development of vaccines based on these virulence characteristics is essential for controlling infection and ensuring long-lasting protection. Various vaccination strategies and formulations have been tested in animal models; however, their effectiveness and reproducibility in humans remain uncertain. Different types of vaccines, including vector-based vaccines, inactivated whole cells, genetically modified protein-based subunits, and multiepitope nucleic acid (DNA) vaccines, have been explored. While some vaccines have demonstrated promising results in murine models, only a limited number have been successfully tested in humans. This article provides a thorough evaluation of recent research on H. pylori virulence genes and vaccination methods, offering valuable insights for future strategies to address this global health challenge.

Background: Helicobacter pylori (HP) is under investigation for its potential role in postoperative complications. While some studies indicate no impact, they often cite short or incomplete follow-up. This study aims to compare 1-year outcomes in groups with and without active HP infection after bariatric surgery, also assessing HP prevalence in postoperative specimens of sleeve gastrectomy (SG) patients. Methods: Conducted between May 2020 and May 2021, this study involves both retrospective and prospective data collection from 93 eligible SG patients. Demographics, surgical outcomes and follow-up results (including complications; weight and BMI at 3, 6 and 12 months post-SG) were extracted. Results: No statistically significant differences in body weight were observed at 3 (p = 0.3757), 6 (p = 0.1422) or 12 (p = 0.2737) months post-surgery between the HP-positive (Group A) and non-infected (Group B) groups. Group A experienced significant reductions in body weight at 6 and 12 months (p < 0.0001), while group B showed significant reductions at 3, 6 and 12 months (p < 0.0001), with additional decreases at 6 and 12 months post-surgery compared to 3 months. No significant differences in overall surgery-related side effects were observed between the groups. Conclusions: Patients with active HP infections undergoing SG displayed comparable rates of short- and long-term complications to the non-infected group. Active HP infection did not impact body weight loss outcomes at 12 months, but it may potentially slow it down in the initial three-month post-surgery period. This underscores the need to consider eradication while maintaining awareness of the potential side effects associated with the process.

Helicobacter pylori (H. pylori), a widely prevalent pathogen that can be cured through relatively simple medical methods, is thought to be potentially associated with the risk of cardiovascular diseases (CVD), although controversy remains. Currently, it is unclear whether the triglyceride-glucose index (TGI), a classic indicator of insulin resistance, influences the relationship between H. pylori infection and CVD. The present work explored the relationships between H. pylori seropositivity, the TGI and CVD, and the potential effect of TGI in this association.

In this cross-sectional and cohort study, data from the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) and NHANES (1999-2000) were used. The effects of the TGI, H. pylori seropositivity, and their interaction on the risk of CVD were assessed using logistic regression models. The hazard ratios (HRs) and 95% confidence intervals (CI) for all-cause mortality (ACM) were calculated using the Cox proportional hazards model. Restricted cubic spline (RCS) curves were employed to investigate potential non-linear or linear relationships among the TGI, H. pylori seropositivity, occurrence of CVD, and ACM. Mediation analyses were employed to assess the potential effects of H. pylori seropositivity and TGI on the risk of CVD and mortality.

Of the 9,399 participants, 4,488 (47.75%) were H. pylori-immunoglobulin G (IgG)-positive, and 3,934 (41.86%) were diagnosed with CVD. In the general population, participants with a TGI ≥ 75th percentile who were positive for H. pylori-IgG antibody had the highest risk of developing CVD (odds ratio = 1.487; 95% CI: 1.088-2.033). Among patients with CVD, those with a TGI ≥ 75th percentile & positive for H. pylori-IgG antibody were at a higher ACM risk (HR = 1.227; 95% CI: 1.009-1.491). H. pylori exhibited a significant mediating effect on CVD occurrence (Pindir = 0.004) and mortality (Pindir = 0.004) via the TGI.

H. pylori seropositivity may indirectly elevate the risk of CVD and mortality via the TGI. Combining the patient's H. pylori serological status with their TGI could enhance the predictive ability for CVD occurrence and related mortality. Therefore, the clinical practice of screening for and eradicating H. pylori in CVD patients may be anticipated.

Three herbal extracts (Asparagus racemosus Willd., Tabebuia avellanedae Lorentz, and Glycyrrhiza glabra L.) were mixed with three essential oils (Foeniculum vulgare Mill., Mentha piperita L., and Pimpinella anisum L.) to formulate a product (HEMEO) whose active compounds include saponins and steroids in Asparagus racemosus, known for their anti-inflammatory properties; glycyrrhizin and flavonoids in Glycyrrhiza glabra, which exhibit gastroprotective and antispasmodic effects; menthol in Mentha piperita, contributing with antispasmodic and antimicrobial properties; and anethole and polyphenols in Pimpinella anisum, which modulate intestinal motility and offer antimicrobial activity.

HEMEO was formulated for applications in intestinal motility disorders.

HEMEO was evaluated for spontaneous and induced motility effects in isolated guinea pig ileum, colon, and stomach. Ex vivo experiments were conducted using LabChart software v7.0, and the product's antibacterial action against Helicobacter pylori and its antioxidant effects were assessed through disc diffusion and FRAP assays. The presence of the volatile compounds in the formulation was confirmed by GC-MS analysis; the TPC of HEMEO, determined using the Folin-Ciocalteu method, was 9.925 ± 0.42 mg GAE/g.

HEMEO showed a phenolic content correlated with its antioxidant potential and in addition inhibited H. pylori growth and demonstrated notable antioxidant properties, suggesting its role as a supportive agent in digestive processes and in managing motility disorders.

Helicobacter pylori (HP), which colonizes exclusively in the gastrointestinal tract, has been reported to dysregulate the immune response and gives rise to several extra-gastrointestinal autoimmune disorders. However, the relationship between HP and immune-mediated ocular diseases remains ambiguous. This study aims to clarify the association between immune-mediated ocular diseases and HP infection, as well as the impact of HP treatment on the incidence of immune-mediated ocular diseases.

This is a retrospective population-based study using National Health Insurance Research Database in Taiwan. Patients with newly diagnosed peptic ulcer disease or HP infection between 2009 and 2015 were identified as HP group and compared to the non-HP group with one-to-one exact matching. Moreover, the incident risk of immune-mediated ocular diseases and its two subgroups (ocular surface and orbital inflammation group, intraocular inflammation group) were compared in HP patients with or without treatment.

A total of 1,030,119 subjects in the non-HP group and 1,030,119 patients in the HP group were enrolled. The incidence rate of immune-mediated ocular diseases was significantly higher in the HP group (95% confidence interval (CI): 2.534-2.547). The incident rate ratio was significantly higher in HP with treatment than without treatment (HR: 1.654, 95% CI: 1.641-1.668). The Cox proportional hazards regression model demonstrated a significantly increased HR of immune-mediated ocular diseases in HP treated group (HR: 2.265, 95% CI: 2.024-2.534) and less increased HR in HP non-treated group (HR: 1.427, 95% CI: 1.273-1.598) when comparing to non-HP group. Subgroup analysis demonstrated a significantly higher incidence rate of ocular surface and orbital inflammation as well as intraocular inflammation in the HP group.

This study illustrated a higher incidence of immune-mediated ocular diseases in HP infection, and a heightened risk following HP eradication.

Helicobacter pylori is a pathogenic bacterium that causes gastritis and gastric carcinoma. Besides gastric complications its potential link with gut-brain axis disruption and neurological disorders has also been reported. The current study investigated the plausible role and its associated molecular mechanism underlying H. pylori mediated gut-brain axis disruption and neuroinflammation leading to neurological modalities like Alzheimer's disease (AD). We have chosen the antimicrobial resistant and susceptible H. pylori strains on the basis of broth dilution method. We have observed the increased inflammatory response exerted by H. pylori strains in the gastric as well as in the neuronal compartment after treatment with Helicobacter pylori derived condition media (HPCM). Further, elevated expression of STAT1, STAT3, and AD-associated proteins- APP and APOE4 was monitored in HPCM-treated neuronal and neuron-astrocyte co-cultured cells. Excessive ROS generation has been found in these cells. The HPCM treatment to LN229 causes astrogliosis, evidenced by increased glial fibrillary acidic protein. Our results indicate the association of STAT3 as an important regulator in the H. pylori-mediated pathogenesis in neuronal cells. Notably, the inhibition of STAT3 by its specific inhibitor, BP-1-102, reduced the expression of pSTAT3 and AD markers in neuronal compartment induced by HPCM. Thus, our study demonstrates that H. pylori infection exacerbates inflammation in AGS cells and modulates the activity of STAT3 regulatory molecules. H. pylori secretome could affect neurological compartments by promoting STAT3 activation and inducing the expression of AD-associated signature markers. Further, pSTAT-3 inhibition mitigates the H. pylori associated neuroinflammation and amyloid pathology.

The gastrointestinal tract (GIT) is an important and complex system by which humans to digest food and absorb nutrients. The GIT is vulnerable to diseases, which may led to discomfort or even death in humans. Therapeutics for GIT disease treatment face multiple biological barriers, which significantly decrease the efficacy of therapeutics. Recognizing the biological barriers and pathophysiological characteristics of GIT may be helpful to design innovative therapeutics. Nanotherapeutics, which have special targeting and controlled therapeutic release profiles, have been widely used for the treatment of GIT diseases. Herein, we provide a comprehensive review of the biological barrier and pathophysiological characteristics of GIT, which may aid in the design of promising nanotherapeutics for GIT disease treatment. Furthermore, several typical diseases of the upper and lower digestive tracts, such as Helicobacter pylori infection and inflammatory bowel disease, were selected to investigate the application of nanotherapeutics for GIT disease treatment.

Helicobacter pylori is a type of Gram-negative microaerobic bacteria that inhabits the gastric mucosal epithelium. It can cause various gastrointestinal diseases including gastritis, peptic ulcer and gastric cancer. White blood cells (WBC) are common immune cells, the increase in whose countoften indicates the presence of an infection. Currently, the relationship between H. pylori and WBC count remains full of controversy. This study aims to further elucidate the effects of H. pylori on WBC count in a population undergoing physical examination.

A total of 864 participants who underwent physical examination and 14C urea breath test (UBT) were retrospectively enrolled in this study from January to June 2021. The overall population was divided into H. pylori-negative (Hp-) and H. pylori-positive (Hp+) groups based on the disintegration per minute (DPM) value detected by UBT. Spearman's correlation analysis was used to assess the correlation between DPM and WBC count. General linear regression models were applied to assess the potential factors contributing to the increase in WBC count. Generalised additive model (GAM) was performed to identify the non-linear relationship between DPM and WBC count. Additionally, a piecewise linear regression was used to examine the threshold effect of the DPM on WBC count.

403 subjects were diagnosed with H. pylori infection. The WBC and platelet (PLT) counts in the Hp+ group were significantly higher than those in the Hp- group. Additionally, the prevalence of H. pylori infection gradually increased with the WBC count quartiles (38.89% and 54.67% in quartile 1 and quartile 4, respectively). Spearman's correlation analysis showed that the DPM value significantly correlated with WBC count (r=0.089, p=0.009) and PLT count (r=0.082, p=0.017). The linear model revealed a positive independent association of H. pylori infection and DPM with WBC count (βHp+=0.398 (95% CI 0.170, 0.625), p<0.001; βDPM=0.002 (95% CI 0.000, 0.0030), p=0.018). The results of the GAM and the piecewise linear regression suggested that the cut-off points of the association between DPM and WBC count were 40 and 155 of DPM, that is, the effect of DPM on WBC count varied with the difference of DPM <40, 40-155, and >155 (βDPM=-0.005 (95% CI -0.017, 0.007), p=0.423; βDPM=0.006 (95% CI 0.002, 0.013), p=0.047; and βDPM=-0.007 (95% CI -0.012, -0.002), p=0.004, respectively).

H. pylori infection was independently and positively correlated with WBC count; however, the effect of DPM on WBC count varied across different WBC count intervals, suggesting distinct immunological responses at different stages of infection.

To explore the application of small-sized magnetically controlled capsule gastroscopy (MCCG) in upper gastrointestinal diseases screening in asymptomatic individuals.

A retrospective analysis of the clinical data of 2163 asymptomatic individuals who underwent small-sized MCCG at our center from September 2022 to December 2023. The detection of submucosal tumors, polyps and ulcers in the upper gastrointestinal tract, the tolerance and safety of the subjects were statistically analyzed.

Suspected submucosal tumors in the upper gastrointestinal tract were detected in 34 (1.57%) of 2136 subjects, with a higher incidence in females and no observed age difference. Polyps were detected in 328 subjects (15.16%), with a higher incidence in females and an increased detection rate with increasing age. Ulcers were detected in 27 subjects (1.25%), with a higher incidence in males and no observed age difference. There was no significant discomfort in all subjects, and no adverse event or capsule retention occurred.

Small-sized MCCG can be used for focal lesion screening in the upper gastrointestinal tract and is comfortable and safe, making it a safe and efficient method for examining upper gastrointestinal diseases in the physical examination population.

In this study we have investigated the effect of chondroitin sulfate-selenium nanoparticles (CS@Se) on Alzheimer's disease (AD) mice using 16S rDNA technique. We randomly divided 30 SPF grade male C57BL/6 J mice into 6 groups according to random number table method. The AD mouse model was established by subcutaneous injection of D-galactose (D-gal) combined with gavage of AlCl3 for 30 consecutive days, and then drug intervention was performed in the administration group for 40 consecutive days. The findings demonstrated several positive effects of CS@Se on AD mice. Firstly, CS@Se improved spatial learning and memory problems and reduces anxiety in AD mice. It also significantly reduced pyramidal cell arrangement disorder and rupture, leading to an improvement in synaptic structure damage between hippocampal neurons. Furthermore, CS@Se reduced mitochondrial swelling and vacuolation while increasing neuron survival in AD mice. Moreover, CS@Se significantly impacted the diversity and richness of intestinal flora in AD mice. It increased the relative abundance of Firmicutes and Actinobacteria while reducing the relative abundance of Bacteroidetes and Proteobacteria. In conclusion, CS@Se effectively reduced the breakdown of hippocampal pyramidal cells, improved the superfiber structure of hippocampal neurons, and restored intestinal flora balance, ultimately contributing to improving learning and memory abilities and alleviating anxiety in AD mice.

Helicobacter pylori (H. pylori) infection may be associated with colorectal polyps/adenomas, but the current evidence remains controversial.

We retrospectively screened the medical records of 655 participants who underwent both colonoscopy and H. pylori test from June 15, 2020 to April 30, 2023. The number, size, location, and pathological type of colorectal polyps/adenomas were compared between H. pylori positive and negative groups. Adjusting for age, gender, smoking, drinking, hypertension, diabetes, fatty liver, body mass index, and inflammatory and metabolic indicators, multivariate logistic regression analyses were performed to evaluate the association of H. pylori infection with the number, size, location, and pathological type of colorectal polyps/adenomas, where no polyp/adenoma was used as reference.

Overall, 508 participants were included, of whom 154 and 354 were divided into H. pylori positive and negative groups, respectively. H. pylori positive group had significantly higher colorectal polyps/adenomas (74.7 % vs. 65.8 %, P=0.048), low-grade adenomas (55.7 % vs. 47.6 %, P=0.026), advanced adenomas (22.6 % vs. 13.3 %, P=0.008), and colorectal polyps/adenomas with sizes of ≥6 mm (61.7 % vs. 48.5 %, P=0.002) and ≥10 mm (25.2 % vs. 14.6 %, P=0.004) than H. pylori negative group. In multivariate logistic regression analyses, H. pylori infection was independently associated with low-grade adenomas (OR=2.677, 95 %CI=1.283-5.587, P=0.009), advanced adenomas (OR=3.017, 95 %CI=1.007-9.036, P=0.049), right-side colon polyps/adenomas (OR=5.553, 95 %CI=1.679-18.360, P=0.005), and colorectal polyps/adenomas with sizes of ≥10 mm (OR=4.436, 95 %CI=1.478-13.310, P=0.008), but not number of colorectal polyps/adenomas.

H. pylori infection is associated with increased risk of colorectal polyps/adenomas, especially low-grade adenomas, advanced adenomas, right-side colon polyps/adenomas, and large colorectal polyps/adenomas.

The aim of this study was to evaluate the effectiveness and safety of the nine most widely studied Vonoprazan (VPZ)-based treatment regimens along with traditional Proton pump inhibitor (PPI)-based treatment regimens in eradicating Helicobacter pylori (H. pylori) infection.

Through searching PubMed, Embase, Cochrane Library, Web of Science, we exclusively included randomized controlled trials (RCTs) to investigate the efficacy of VPZ-based and PPI-based therapies for H. pylori infection. The included studies were evaluated for methodological quality using the Cochrane bias risk assessment tool, and the data analysis software was used to analyze the data accordingly.

The RCTs were collected from the earliest available date up to August 2023. Twenty-one RCTs were included, with a total sample size of 5481. The results of the network meta-analysis showed that the eradication rate of the VPZ-based quadruple 14-day (VPZ-Q14) treatment regimen in Intention-to-treat (ITT) analysis was the highest (SUCRA: 0.874); The eradication rate of the VPZ-based quadruple 10-day (VPZ-Q10) treatment plan in Per-protocol (PP) analysis was the highest (SUCRA: 0.849). All regimens were well tolerated without significant differences. According to the probability ranking of safety, high-dose VPZ-based dual 14-day therapy (H-VPZ-D14) ranked first in SUCRA, reaching 0.952. This indicates that H-VPZ-D14 treatment is the safest with a relatively low incidence of adverse effect. Therefore, VPZ-based therapies not only have a higher eradication rate, but also possess satisfactory safety.

Compared with traditional PPI-based therapies, VPZ-based therapies have shown superior eradication effects. Based on the Ranking Plot of the Network, the VPZ-Q14 or VPZ-Q10 treatment regimen for H. pylori has a higher eradication rate and acceptable differences compared to other treatment regimens. In addition, for regions with high antibiotic resistance rates, we recommend a 14-day quadruple therapy with bismuth based on VPZ.

Helicobacter pylori is a prevalent, global infectious disease that causes dyspepsia, peptic ulcer disease, and gastric cancer. The American College of Gastroenterology commissioned this clinical practice guideline (CPG) to inform the evidence-based management of patients with H. pylori infection in North America. This CPG used Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology to systematically analyze 11 Population, Intervention, Comparison, and Outcome questions and generate recommendations. Where evidence was insufficient or the topic did not lend itself to GRADE, expert consensus was used to create 6 key concepts. For treatment-naive patients with H. pylori infection, bismuth quadruple therapy (BQT) for 14 days is the preferred regimen when antibiotic susceptibility is unknown. Rifabutin triple therapy or potassium-competitive acid blocker dual therapy for 14 days is a suitable empiric alternative in patients without penicillin allergy. In treatment-experienced patients with persistent H. pylori infection, "optimized" BQT for 14 days is preferred for those who have not been treated with optimized BQT previously and for whom antibiotic susceptibility is unknown. In patients previously treated with optimized BQT, rifabutin triple therapy for 14 days is a suitable empiric alternative. Salvage regimens containing clarithromycin or levofloxacin should only be used if antibiotic susceptibility is confirmed. The CPG also addresses who to test, the need for universal post-treatment test-of-cure, and the current evidence regarding antibiotic susceptibility testing and its role in guiding the choice of initial and salvage treatment. The CPG concludes with a discussion of proposed research priorities to address knowledge gaps and inform future management recommendations in patients with H. pylori infection from North America.

Helicobacter pylori infection has significant epidemiological relevance due to the carcinogenic nature of this bacterium, which is potentially associated with cancer. When detected, it should ideally be eradicated using a treatment that currently involves a combination of gastric acid suppressors and multiple antibiotics. However, this treatment raises questions regarding efficacy and safety profiles in patients with specific comorbidities, including inflammatory bowel diseases (IBD). Eradication therapy for H. pylori includes components associated with adverse gastrointestinal events, such as Clostridioides difficile colitis. This necessitates quantifying this risk through dedicated studies to determine whether this antimicrobial treatment could be significantly associated with IBD relapse or exacerbation of pre-existing IBD, as well as whether it could potentially lead to the de novo onset of IBD. Although the available evidence is reassuring about the safety of eradication therapy in patients with IBD, it is limited, and there are no specific recommendations for this particular situation in the leading international IBD and H. pylori guidelines. Therefore, studies need to evaluate the efficacy and safety profiles of the available antimicrobial regimens for H. pylori eradication in patients with IBD, both in clinical trial settings and in real-life studies.

Helicobacter pylori (H. pylori) is responsible for various chronic or acute diseases, such as stomach ulcers, dyspepsia, peptic ulcers, gastroesophageal reflux, gastritis, lymphoma, and stomach cancers. Although specific drugs are available to treat the bacterium's harmful effects, there is an urgent need to develop a preventive or therapeutic vaccine. Therefore, the current study aims to create a multi-epitope vaccine against H. pylori using lipid nanoparticles. Five epitopes from five target proteins of H. pylori, namely, Urease, CagA, HopE, SabA, and BabA, were used. Immunogenicity, MHC (Major Histocompatibility Complex) bonding, allergenicity, toxicity, physicochemical analysis, and global population coverage of the entire epitopes and final construct were carefully examined. The study involved using various bioinformatic web tools to accomplish the following tasks: modeling the three-dimensional structure of a set of epitopes and the final construct and docking them with Toll-Like Receptor 4 (TLR4). In the experimental phase, the final multi-epitope construct was synthesized using the solid phase method, and it was then enclosed in lipid nanoparticles. After synthesizing the construct, its loading, average size distribution, and nanoliposome shape were checked using Nanodrop at 280 nm, dynamic light scattering (DLS), and atomic force microscope (AFM). The designed vaccine has been confirmed to be non-toxic and anti-allergic. It can bind with different MHC alleles at a rate of 99.05%. The construct loading was determined to be about 91%, with an average size of 54 nm. Spherical shapes were also observed in the AFM images. Further laboratory tests are necessary to confirm the safety and immunogenicity of the multi-epitope vaccine.

H. pylori infection is gaining increasing attention, but detailed investigations into its impact on gastric microbiota remain limited. We collected gastric mucosa samples from 47 individuals divided into three groups: 1. Group HP: patients with initial positive H. pylori infection (25 cases); 2. Group ck: H. pylori-negative patients (14 cases); 3. Group DiffHP: patients with refractory H. pylori infection (8 cases). The samples were analyzed using 16S rDNA sequencing and functional prediction with PICRUSt. Group HP showed differences in flora distribution and function compared to Group ck, while Group DiffHP overlapped with Group HP. The abundances of Aeromonas piscicola, Shewanella algae, Vibrio plantisponsor, Aeromonas caviae, Serratia marcescens, Vibrio parahaemolyticus, Microbacterium lacticum, and Prevotella nigrescens were significantly reduced in both Group DiffHP and Group HP compared to Group ck. Vibrio shilonii was reduced only in Group DiffHP compared to Group ck, while Clostridium perfringens and Paracoccus marinus were increased only in Group DiffHP. LEfSe analysis revealed that Clostridium perfringens and Paracoccus marinus were enriched, whereas Vibrio shilonii was reduced in Group DiffHP compared to Group ck at the species level. In individuals with refractory H. pylori infection, the gastric microbiota exhibited enrichment in various human diseases, organic systems, and metabolic pathways (amino acid metabolism, carbohydrate metabolism, transcription, replication and repair, cell cycle pathways, and apoptosis). Patients with multiple failed H. pylori eradication exhibited significant changes in the gastric microbiota. An increase in Clostridium perfringens and Paracoccus marinus and a decrease in Vibrio shilonii appears to be characteristic of refractory H. pylori infection.

Recent observational studies examining the association between Helicobacter pylori infection and the risk of metabolic dysfunction-associated steatotic liver disease (MASLD) have reported conflicting results. We performed a meta-analysis to quantify the magnitude of the association between H. pylori infection and the risk of MASLD.

We systematically searched three large electronic databases to identify eligible observational studies (published up to 30 November 2023) in which liver biopsy, imaging methods or blood-based biomarkers/scores were used for diagnosing MASLD. Data from selected studies were extracted, and meta-analysis was performed using common and random-effects modelling. Statistical heterogeneity among published studies, subgroup analyses, meta-regression analyses and publication bias were assessed.

A total of 28 observational studies (24 cross-sectional and 4 longitudinal studies) were identified, including 231 291 middle-aged individuals of predominantly Asian ethnicity (~95%). Meta-analysis of cross-sectional studies showed that H. pylori infection was significantly associated with a small increase in the risk of prevalent MASLD (n = 24 studies; random-effects odds ratio 1.11, 95% CI 1.05-1.18; I2 = 63%). Meta-analysis of data from longitudinal studies showed that H. pylori infection was significantly associated with an increased risk of developing incident MASLD over a mean 5-year follow-up (n = 4 studies; random-effects odds ratio 1.20, 95%CI 1.08-1.33; I2 = 44%). Sensitivity analyses did not modify these results. The funnel plot did not reveal any significant publication bias.

H. pylori infection is associated with a mildly increased risk of prevalent and incident MASLD. Further well-designed prospective and mechanistic studies are required to better decipher the complex link between H. pylori infection and the risk of MASLD.

Helicobacter pylori is a type of Gram-negative bacteria belonging to the Proteobacteria phylum which is known to cause gastrointestinal disorders such as gastritis and gastric ulcers. Its treatment is based on current eradication regimens, which are composed of combinations of antibiotics such as clarithromycin, metronidazole, levofloxacin and amoxicillin, often combined with a proton pump inhibitor (PPI). With the development of sequencing technologies, it has been demonstrated that not only does the colonization of the gastric and gut environment by H. pylori cause microbial changes, but also the treatment regimens used for its eradication have a significant altering effect on both the gastric and gut microbiota. Here, we review current knowledge on microbiota modulations of current therapies in both environments. We also summarize future perspectives regarding H. pylori infection, the integration of probiotics into therapy and what challenges are being faced on a global basis when we talk about eradication.

Helicobacter pylori is a gastric oncopathogen that infects over half of the world's human population. It is a Gram-negative, microaerophilic, helix-shaped bacterium that is equipped with flagella, which provide high motility. Colonization of the stomach is asymptomatic in up to 90% of people but is a recognized risk factor for developing various gastric disorders such as gastric ulcers, gastric cancer and gastritis. Invasion of the human stomach occurs via numerous virulence factors such as CagA and VacA. Similarly, outer membrane proteins (OMPs) play an important role in H. pylori pathogenicity as a means to adapt to the epithelial environment and thereby facilitate infection. While some OMPs are porins, others are adhesins. The epithelial cell receptors SabA, BabA, AlpA, OipA, HopQ and HopZ have been extensively researched to evaluate their epidemiology, structure, role and genes. Moreover, numerous studies have been performed to seek to understand the complex relationship between these factors and gastric diseases. Associations exist between different H. pylori virulence factors, the co-expression of which appears to boost the pathogenicity of the bacterium. Improved knowledge of OMPs is a major step towards combatting this global disease. Here, we provide a current overview of different H. pylori OMPs and discuss their pathogenicity, epidemiology and correlation with various gastric diseases.

Helicobacter pylori is an important public health concern due to its status as a carcinogenic bacterium. Well adapted to the acidic environment of the human stomach, the variety of strains and virulence factors of the organism when interacting with the host immune system creates an individualistic response. Although estimates suggest that approximately half of the global population is infected with H pylori, the majority of infected persons remain asymptomatic while harboring an increased risk of intestinal metaplasia and gastric cancers. Therefore, appropriate diagnostic testing protocols are imperative.

This study compared labeling methodologies, including Wright stain, alcian yellow toluidine blue (AYTB), and immunohistochemistry (IHC) on formalin-fixed paraffin-embedded stomach resections from sleeve gastrectomy patients, to detect H pylori infection.

Although all 3 labeling methods evidenced similar specificity in H pylori detection, the IHC method was significantly more sensitive. However, the IHC cost per test was approximately 5-fold higher than that of the Wright or AYTB stains, and the technical time required per test was at least 6-fold that of Wright or AYTB.

Despite the higher cost per test, IHC is the most sensitive and preferred method for determination of H pylori infection.

Helicobacter pylori infection is acquired in childhood via the oral cavity, although its relationship with the characteristics of the oral microbiome has not been elucidated. In this study, we performed comprehensive analysis of the oral microbiome in children and adults with or without H. pylori in the oral cavity.

Bacterial DNA was extracted from 41 adult and 21 child saliva specimens, and H. pylori was detected using PCR. 16S rRNA gene amplification was performed for next-generation sequencing. Bioinformatic analyses were conducted using Quantitative Insights into Microbial Ecology 2 (QIIME 2).

Faith's phylogenetic diversity analysis showed a significant difference between H. pylori-negative adult and child specimens in terms of α-diversity (p < 0.05), while no significant difference was observed between H. pylori-positive adult and child specimens. There was also a significant difference in β-diversity between H. pylori-positive and negative child specimens (p < 0.05). Taxonomic analysis at the genus level revealed that Porphyromonas was the only bacterium that was significantly more abundant in both H. pylori-positive adults and children than in corresponding negative specimens (p < 0.01 and p < 0.05, respectively).

These results suggest unique oral microbiome characteristics in children with H. pylori infection in the oral cavity.

Helicobacter pylori (H. pylori) antibiotic resistance is the leading cause for unsuccessful eradication therapy. After one or more failures, the chance of encountering secondary antibiotic resistance increases. The aim of this study was to characterize genotypic secondary resistance in a cohort of southern Italian H. pylori patients with at least one previous failure. Such patients collected stool samples using a dedicated kit (THD fecal testTM), and bacterial DNA was extracted and amplified using RT-PCR. Resistance to clarithromycin, amoxicillin, metronidazole, levofloxacin, and tetracycline was assessed using a high-resolution melting curve. We enrolled 50 patients. A total of 72% of patients failed one previous antibiotic course, 16% failed two, 10% failed three, and 2% failed four. The rate of secondary antibiotic resistance was 16% for clarithromycin, 18% for metronidazole, 14% for amoxicillin, 14% for levofloxacin, and 2% for tetracycline. Among the eight clarithromycin-resistant patients, five (62.5%) previously received a clarithromycin-based regimen. The same rate was 33.3% (3/9) for metronidazole. The only tetracycline-resistant patient had received Pylera. In conclusion, our data seem to show that, even though secondary resistance is not very high, resistance to clarithromycin could be very likely related to previous exposure to this antibiotic.

This study aims to comprehensively review the multifaceted factors underlying the successful colonization and infection process of Helicobacter pylori (H. pylori), a prominent Gram-negative pathogen in humans. The focus is on elucidating the functions, mechanisms, genetic regulation, and potential cross-interactions of these elements.

Employing a literature review approach, this study examines the intricate interactions between H. pylori and its host. It delves into virulence factors like VacA, CagA, DupA, Urease, along with phase variable genes, such as babA, babC, hopZ, etc., giving insights about the bacterial perspective of the infection The association of these factors with the infection has also been added in the form of statistical data via Funnel and Forest plots, citing the potential of the virulence and also adding an aspect of geographical biasness to the virulence factors. The biochemical characteristics and clinical relevance of these factors and their effects on host cells are individually examined, both comprehensively and statistically.

H. pylori is a Gram-negative, spiral bacterium that successfully colonises the stomach of more than half of the world's population, causing peptic ulcers, gastric cancer, MALT lymphoma, and other gastro-duodenal disorders. The clinical outcomes of H. pylori infection are influenced by a complex interplay between virulence factors and phase variable genes produced by the infecting strain and the host genetic background. A meta-analysis of the prevalence of all the major virulence factors has also been appended.

This study illuminates the diverse elements contributing to H. pylori's colonization and infection. The interplay between virulence factors, phase variable genes, and host genetics determines the outcome of the infection. Despite biochemical insights into many factors, their comprehensive regulation remains an understudied area. By offering a panoramic view of these factors and their functions, this study enhances understanding of the bacterium's perspective, i.e. H. pylori's journey from infiltration to successful establishment within the host's stomach.