Gut Pathogens最新文献

{"title":"Serial serum interleukin-8 trajectories are associated with progression from Helicobacter pylori-associated precancerous lesions to gastric cancer: a prospective longitudinal cohort study.","authors":"Atteyat A Semeya, Raafat S A Abdel Hafez, Rasha Elgamal, Abeer Badr, Mahmoud Ibrahim Orabi, Shimaa R Younis, Mahmoud M Morgan, Mahmoud Ahmed Hassan, Mohamed Ramzy Alawy, Amira A A Othman","doi":"10.1186/s13099-026-00876-8","DOIUrl":"10.1186/s13099-026-00876-8","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer remains the fourth leading cause of cancer-related mortality worldwide, with delayed diagnosis contributing to poor prognosis. Current biomarkers lack sensitivity for early detection. Interleukin-8 (IL-8), a pro-inflammatory chemokine implicated in H. pylori-associated gastric carcinogenesis, has not been rigorously evaluated in longitudinal studies for its ability to predict malignant progression in patients with precancerous lesions.</p><p><strong>Aim: </strong>To investigate whether serial serum IL-8 measurements predict progression to gastric cancer among Egyptian patients with H. pylori-associated atrophic gastritis and intestinal metaplasia over 24 months of follow-up.</p><p><strong>Methods: </strong>a prospective, longitudinal biomarker, multicenter cohort study enrolled 200 participants across 5 Egyptian centers: 50 with atrophic gastritis, 50 with intestinal metaplasia, 25 with H. pylori-positive gastric cancer, 25 with H. pylori-negative gastric cancer, and 50 healthy controls. All underwent baseline clinical assessment, laboratory evaluation (including CEA, CA19-9), H. pylori testing (stool antigen and urea breath test per Maastricht VI), and endoscopy with histopathology (Updated Sydney System). Patients with precancerous lesions were followed for 24 months with serial IL-8 measurements at 0, 6, 12, 18, and 24 months, and repeat endoscopy at study completion. Group-based trajectory modeling was performed blinded to outcome status. Multivariable logistic regression with penalization was used due to low event count. Time-dependent ROC analysis used a cumulative/dynamic approach.</p><p><strong>Results: </strong>Of 100 patients with precancerous lesions, 94 completed follow-up, and 9 progressed to gastric cancer (7 from intestinal metaplasia, 2 from atrophic gastritis). Baseline IL-8 levels demonstrated a progressive increase across groups (controls: 9.7 ± 3.2 pg/mL; atrophic gastritis: 42.1 ± 11.8; intestinal metaplasia: 64.8 ± 14.3; gastric cancer: 107.4 ± 24.6; p < 0.001). IL-8 elevation in gastric cancer was independent of H. pylori status across all stages (p > 0.50 for all stage-stratified comparisons, though these subgroup analyses are limited by small sample sizes and may be considered exploratory). Baseline IL-8 > 52.3 pg/mL was associated with progression risk, AUC 0.84, sensitivity 88.9%, specificity 78.0%, and negative predictive value 98.5%, significantly outperforming CEA (AUC 0.62) and CA19-9 (AUC 0.58). Time-dependent AUC increased to 0.91 at 12 months and 0.94 at 18 months. Trajectory modeling, performed blinded to outcome, identified three patterns: Stable-Low (n = 42), Moderate-Rising (n = 49), and High-Accelerating (n = 9). The acceleration point in the High-Accelerating group preceded clinical cancer diagnosis by a median of 6 months (range 3-12), however, this exploratory finding requires external validation. In multivariable analysis using Firth penalized regression, ba","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levofloxacin-based concomitant versus sequential therapy for Helicobacter pylori eradication in treatment-naïve Syrian patients: a randomized trial showing no superiority of sequential therapy.","authors":"Marouf Alhalabi, Hussam Aldeen Alshiekh, Alaa Aldeen Sheikh Alhara, Wael Shehab","doi":"10.1186/s13099-026-00881-x","DOIUrl":"10.1186/s13099-026-00881-x","url":null,"abstract":"<p><strong>Background: </strong>Helicobacter pylori (H. pylori) infection remains highly prevalent worldwide, including the Eastern Mediterranean region. In Syria, standard triple therapy effectiveness has declined due to increasing antibiotic resistance, misuse, and healthcare limitations. As susceptibility-guided therapy and recommended regimens may be unavailable, empirical levofloxacin-based therapies remain used. This randomized trial compared two levofloxacin-based regimens under local conditions, as sequential therapy has not been evaluated previously in Syrian patients.</p><p><strong>Methods: </strong>This single-center, prospective, open-label, randomized superiority trial included 150 treatment-naïve adults with histologically confirmed H. pylori infection. Participants were assigned equally to receive either a 14-day levofloxacin-based concomitant regimen or a 14-day levofloxacin-based sequential regimen. The primary outcome was eradication success, confirmed by negative stool antigen testing 6 weeks after therapy and analyzed using intention-to-treat analysis. Treatment-related adverse events were recorded.</p><p><strong>Results: </strong>Intention-to-treat eradication rates were 84%(63/75) with concomitant therapy and 81.3%(61/75) with sequential therapy. The risk difference was 2.7% points (95%CI:-9.4 to 14.8), with no significant difference between groups (p = 0.83;OR = 1.20(95% CI:0.516-2.81). Baseline characteristics were comparable. Both regimens were generally well tolerated. Nausea was the most frequent adverse event, followed by anorexia, headache, bitter taste, and skin rash, with no significant difference in adverse event frequency.</p><p><strong>Conclusion: </strong>Levofloxacin-based sequential therapy was not superior to concomitant therapy for eradication in treatment-naïve Syrian patients. The lack of a statistically significant difference does not establish equivalence or non-inferiority. Both regimens showed moderate effectiveness. When levofloxacin-based therapy is required due to limited alternatives, the simpler concomitant regimen may offer practical advantages. These findings should be interpreted considering local resistance patterns and healthcare limitations, with further multi-center studies incorporating susceptibility testing needed.</p><p><strong>Clinical trial registration: </strong>ClinicalTrials.gov (NCT06065267), prospectively registered on October 3, 2023.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Prevalence and pathologic effects of colibactin and cytotoxic necrotizing factor‑1 (Cnf 1) in Escherichia coli: experimental and bioinformatics analyses.","authors":"Radwa N Morgan, Sarra E Saleh, Hala A Farrag, Mohammad M Aboulwafa","doi":"10.1186/s13099-026-00882-w","DOIUrl":"10.1186/s13099-026-00882-w","url":null,"abstract":"","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13587435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the dynamics of antibiotic resistance genes in the human gut microbiome across populations.","authors":"Deepika Pateriya, Anjli Tanwar, Vineet K Sharma","doi":"10.1186/s13099-026-00860-2","DOIUrl":"10.1186/s13099-026-00860-2","url":null,"abstract":"<p><p>The human microbiome serves as a reservoir of antibiotic resistance genes (ARGs), collectively known as the resistome, which has crucial implications for human health. However, the distribution of ARGs across diverse bacterial taxa and their variation across populations, disease states, and body sites remain less well understood. Here, we comprehensively profiled the human resistome using genomic and metagenomic data. Our analysis included 4,744 species-representative gut bacterial genomes and 452 oral bacterial genomes, along with gut metagenomic data from 10,230 individuals across 58 studies encompassing 5,388 healthy and 4,842 disease-associated samples, including underexplored non-Western cohorts. Our analysis revealed variation in the gut resistome across population groups and countries. The oral microbiome exhibited a distinct resistome profile with lower ARG prevalence compared to the gut. Across multiple datasets, ARG abundance was generally higher in inflammatory bowel disease samples compared to healthy samples. Pathogenic taxa such as Enterobacter, Citrobacter, Escherichia, and Klebsiella carried the highest number of ARGs, including clinically relevant ARGs, whereas abundant commensals like Bacteroides and Prevotella contributed to the baseline resistome. Notably, population-level differences in ARG composition appeared to be linked to microbial community structure. Shared ARGs between commensal and pathogenic bacteria provided clues to horizontal gene transfer. These findings provide crucial insights into the ecological and population-level factors shaping the gut resistome, highlighting the roles of both pathogens and commensals in the maintenance and dissemination of antimicrobial resistance.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiome dysbiosis in long COVID: a scoping review of mechanistic insights, symptom associations, and therapeutic targets.","authors":"Leonardo Cano-Cevallos, Gabriela Patiño-Aveiga, Alice Gaibor-Pazmiño, Esteban Ortiz-Prado, Juan S Izquierdo-Condoy","doi":"10.1186/s13099-026-00853-1","DOIUrl":"10.1186/s13099-026-00853-1","url":null,"abstract":"<p><strong>Background: </strong>The human microbiome, particularly the gut microbiome, plays a critical role in host immunity, metabolism, and barrier function. Emerging evidence suggests that persistent alterations in microbiome composition-termed dysbiosis-may contribute to the development and symptom persistence of Long COVID.</p><p><strong>Aims: </strong>To map the available literature on microbiome dysbiosis in relation to Long COVID, identify key microbial alterations, associated symptoms, and evaluate potential microbiome-targeted interventions.</p><p><strong>Materials and methods: </strong>The scoping review followed Joanna Briggs Institute (JBI) methodological guidance and was reported according to PRISMA-ScR. A comprehensive search of PubMed, Scopus, Web of Science, and Cochrane Library databases was conducted for studies published from January 2000 to May 2025. Eligible studies included human subjects with a clinical diagnosis of Long COVID and microbiome-related outcomes. Data was charted using a standardized form and synthesized narratively and descriptively.</p><p><strong>Results: </strong>A total of 62 sources were included, most of which were narrative, conceptual, or descriptive in nature. The available literature most frequently discussed gut microbiome dysbiosis in relation to Long COVID, including reduced abundance of beneficial taxa such as Faecalibacterium prausnitzii and Bifidobacterium adolescentis, and increased abundance of opportunistic or pro-inflammatory taxa such as Ruminococcus gnavus and Clostridium innocuum. Reported or proposed associations involved fatigue, gastrointestinal symptoms, neuropsychiatric manifestations, and immune dysregulation. Evidence from respiratory and oral microbiomes was more limited. Microbiome-targeted interventions, including probiotics, prebiotics, synbiotics, diet, and fecal microbiota transplantation (FMT), were mainly proposed or discussed, with limited direct interventional evidence.</p><p><strong>Conclusions: </strong>Current evidence suggests that microbiome alterations may be associated with Long COVID, but the available literature remains largely descriptive, observational, and hypothesis-generating. Further longitudinal and interventional studies are needed to clarify causality and determine whether microbiome-targeted strategies have therapeutic value.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demographic characteristics and associated conditions in enteropathogenic Escherichia coli positive patients.","authors":"Heather Lusby, Stacy G Beal, Kenneth H Rand","doi":"10.1186/s13099-026-00864-y","DOIUrl":"https://doi.org/10.1186/s13099-026-00864-y","url":null,"abstract":"<p><strong>Background: </strong>Many studies have examined the epidemiology and risk factors of Enteropathogenic Escherichia coli (EPEC); however, few have focused on the adult population. This study aimed to determine if EPEC was associated with certain patient populations or characteristics. We reviewed 792 hospitalized adults and children with symptomatic diarrhea who tested positive for EPEC on the BioFire Gastrointestinal (GI) Pathogen Panel and compared with symptomatic patients with no targets detected on the same panel as controls.</p><p><strong>Results: </strong>In the adult group the EPEC positive actual length of stay (LOS) was 13.5 days CI 95% [4.6,22.2] vs. 9.3 days CI 95% [7.9,10.5] (p = 0.14) for the control group, while in the pediatric population, both expected and actual LOS were actually longer in the EPEC negative patients than the EPEC positive patients (p ≤ 0.01 for both). In adults, 31.4% of EPEC positive patients had a past medical history of autoimmune disease, compared to 19.2% (p = 0.03) in the control group, after controlling for multiple variable testing.</p><p><strong>Conclusion: </strong>To our knowledge, this association between EPEC and autoimmune disease has not been previously reported and could be mediated by gut dysbiosis, suggesting avenues for follow up studies.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13483709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative genomics of Bifidobacterium crudilactis NASR_001 - unveiling the tapestry of a putative probiotic.","authors":"Sneha Kedia, Pittu Sandhya Rani, Mahanga Nyambero, Viraj Bandsode, Vidyullatha Peddireddy, Niyaz Ahmed","doi":"10.1186/s13099-026-00861-1","DOIUrl":"10.1186/s13099-026-00861-1","url":null,"abstract":"<p><strong>Background: </strong>Bifidobacteria are the initial colonizers of the human gastrointestinal tract. Due to an obligate anaerobic character, the isolation and culture of Bifidobacterium spp. is challenging. This bottleneck has led to studies being focused on metagenomic analysis rather than genome sequencing of Bifidobacterium spp. from pure cultures. Our metadata analysis revealed paucity of Bifidobacterium genomes reported from the Indian subcontinent. In this report, we describe the selective isolation and whole genome sequencing (WGS) of Bifidobacterium crudilactis from a pure culture of dairy origin from India.</p><p><strong>Results: </strong>The WGS by Oxford Nanopore long-read sequencing of genomic DNA of B. crudilactis isolate NASR_001 revealed a single circular chromosome of 2,347,652 bp with a GC content of 57.5%. Genome annotation predicted 1923 coding sequences, 6 rRNAs, 46 tRNAs with no CRISPR arrays. Moreover, average nucleotide identity (ANI) analysis with B. crudilactis LMG 23 609 (RefSeq accession GCF_000738005.1) and B. crudilactis MAG UW_FK_BIF1_1 (RefSeq accession GCF_047836735.1) showed 98.8% and 97.3% similarity, respectively, revealing thereby a closest identity and functional similarity to B. crudilactis. The presence of genetic attributes for carbohydrate metabolism, stress response genes and absence of antimicrobial resistance (AMR) encoding genes, as well as paucity of virulence genes signify B. crudilactis NASR_001 to be a putative probiotic organism.</p><p><strong>Conclusion: </strong>The genome sequence of B. crudilactis NASR_001 represents a high-quality genome, representative of the species. It offers valuable insights for further exploration of its promising probiotic potential and functional characteristics.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"18 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current and emerging therapeutic strategies targeting adherent-invasive Escherichia coli in Crohn's disease: a review.","authors":"Layla Ahmed Mohammed Abdelhadi, Yan Liang, Yuexia Liao, Guoqiang Zhu","doi":"10.1186/s13099-026-00852-2","DOIUrl":"10.1186/s13099-026-00852-2","url":null,"abstract":"<p><p>Considerable evidence has accumulated over the past two decades demonstrating that Escherichia coli, specifically adherent-invasive E. coli, contributes to the pathogenesis of Crohn's disease. Adherent-invasive E. coli can adhere to and invade intestinal epithelial cells, survive, and replicate within macrophages, thereby enabling a key mechanism that induces chronic inflammation. Despite extensive knowledge of the molecular interactions between adherent-invasive E. coli and the host from these studies, translating this knowledge into targeted therapy remains limited.In this review, we summarize current and proposed treatments to prevent or eliminate adherent-invasive E. coli colonization. We provide a theoretical framework that categorizes these strategies into four main pillars: direct pathogen targeting (e.g., antibiotics, phage therapy), blockade of bacterial virulence factors (e.g., anti-adhesive compounds, QseC inhibitors), host-mediated clearance (e.g., autophagy inducers), and ecological intervention/restoration (e.g., fecal microbiota transplantation, Probiotic, Prebiotic and Probiotics). Finally, we discuss new modalities, including predatory bacteria, siderophore immunization, and other approaches. This review identifies the latest weapons against adherent-invasive E. coli, synthesizes experimental and clinical evidence to provide a comprehensive view of this evolving therapeutic arsenal, and offers ideas for future treatment of Crohn's disease.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota-derived metabolite landscapes modulate Fusobacterium fitness and colorectal cancer cell behaviour.","authors":"Chhavi Dhiman, Abhiram Kumar, Shreya S Sonak, Priyanka Erukulla, Vijaykumar Dayaram Nimbarte, Kumar Pranav Narayan","doi":"10.1186/s13099-026-00859-9","DOIUrl":"10.1186/s13099-026-00859-9","url":null,"abstract":"<p><strong>Background: </strong>Gut microbiota dysbiosis is increasingly viewed as a disruption of microbial metabolic functions rather than only a shift in microbial composition. Microbiota-derived metabolites not only shape microbial ecology but also directly influence surrounding host tissues by modulating epithelial cell signaling, inflammation, and tumor-associated processes. Among dysbiosis-associated microbes, Fusobacterium is consistently enriched in colorectal cancer (CRC) and contributes to tumor progression, yet the ecological factors regulating its expansion and interaction with host tissues remain unclear. Here, we investigated how microbiome-derived metabolite environments associated with healthy and dysbiotic microbial communities influence Fusobacterium fitness and colorectal epithelial cell behavior.</p><p><strong>Methods: </strong>CRC-associated dysbiosis was generated using an orthotopic murine CRC model combined with antibiotic-induced microbiota perturbation. Gut microbial communities were profiled using 16 S rRNA gene sequencing. Metabolite-enriched supernatants derived from healthy gut microbiota, oral microbiota, dysbiotic microbiota and probiotic cultures were evaluated for their effects on CRC-associated bacteria and Fusobacterium sp. growth, adhesion and invasion. These metabolite supernatants were applied to colorectal cancer cells and their effects on viability (MTT assay), migration (scratch assay), apoptosis (Annexin V-FITC flow cytometry), and inflammatory signaling (Western blot analysis of inflammatory markers) were evaluated.</p><p><strong>Results: </strong>CRC-associated dysbiosis showed reduced microbial diversity with enrichment of opportunistic taxa including Fusobacterium and depletion of beneficial commensals such as Lactobacillus and Bifidobacterium. Metabolite-enriched supernatants from healthy gut and oral microbiota suppressed Fusobacterium growth by 55-65% and reduced bacterial adhesion and invasion in epithelial cells. In epithelial models, these metabolite environments reduced CRC viability to 60% of untreated control, with comparatively smaller effects observed in non-cancerous epithelial cells. They also inhibited cell migration, accompanied by suppression of inflammatory signaling pathways including IL-6, IL-1β, NF-κB, and HIF-1α. In contrast, conditioned media from dysbiotic cancer-microbiota interactions increased tumor cell viability to 120-140% of controls. These findings suggest an association between microbiota-derived metabolite landscapes, pathobiont fitness and epithelial responses under CRC-associated dysbiosis.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental regulation of virulence in Vibrio cholerae: integrating multi-omics, predictive models, and comparative insights across emerging Vibrio species.","authors":"Seyed Soheil Tabibian, Shayan Yaghmayee, Aryan Rahbar, Ava Khalili Dehkordi, Samira Sanami, Omid Pajand","doi":"10.1186/s13099-026-00858-w","DOIUrl":"10.1186/s13099-026-00858-w","url":null,"abstract":"<p><p>Vibrio cholerae thrives at the interface between the aquatic environment and the human host dynamically through integration of environmental signals to highly coordinated virulence programs. This review examines how environmental sensing systems, regulatory networks, biofilm formation, and secretory systems have been integrated to maintain stability, transmission, and pathogenesis. By incorporating these advances in genomics, transcriptomics, proteomics, metabolomics, and predictive models, we demonstrate how multi-omics approaches have changed our understanding of condition-related virulence regulation at the system-level view. In addition, we extend this framework via comparative analysis among pathogenic Vibrio species and also reveal conserved regulatory architectures alongside species-specific adaptations that affect ecological fitness and pathological potential. Finally, discussing how multi-omics and machine learning integration can enable outbreak prediction, inform One Health approaches, and identify environmental regulating anti-virulence targets. This integrated insight positions environmental regulation as a central organizing agent of Vibrio pathogenicity and provides a roadmap for translating complex biological datasets to practical insights in the public health and treatment field.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13628955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}