Gut PathogensPub Date : 2025-12-08DOI: 10.1186/s13099-025-00783-4
Tianze Shang, Rui Zhang, Yani Liu, Shaojun Shi
{"title":"Intestinal oxygen and microbiota crosstalk: implications for pathogenesis of gastrointestinal diseases and emerging therapeutic strategies.","authors":"Tianze Shang, Rui Zhang, Yani Liu, Shaojun Shi","doi":"10.1186/s13099-025-00783-4","DOIUrl":"10.1186/s13099-025-00783-4","url":null,"abstract":"<p><p>The gut microbiota and its hypoxic host environment play a critical role in human health. Despite its importance, the mechanisms maintaining homeostasis and the characteristics defining dysbiosis remain largely undefined. In particular, the regulation of intestinal oxygen (IO) levels emerges as a critical factor in maintaining microbial balance. Host-driven factors, including epithelial oxygen consumption, mucosal perfusion, and luminal gas diffusion, establish a hypoxic gradient essential for the stable colonization by obligate anaerobes. Disruptions to this gradient, leading to pathological hyperoxia, are associated with overgrowth of facultative anaerobic bacteria and contribute to gastrointestinal diseases like ulcerative colitis, colorectal cancer, and irritable bowel syndrome. Emerging therapeutic approaches focus on modulating IO homeostasis to address dysbiosis. Compounds like sodium tungstate inhibit microbial respiratory pathways, while PPAR-γ agonists enhance mitochondrial efficiency in colonic epithelial cells, thereby restoring proper hypoxia. Dietary interventions and probiotic therapies also hold promise by promoting local anaerobic conditions and enhancing barrier functions, thus supporting the restoration of a healthy microbial community. This review highlights the role of IO in shaping host-microbe interactions, focusing on how host IO levels influence microbial homeostasis. We evaluate the potential for IO modulation to improve gut microbiota structure and explore its impact on microbial metabolism and disease pathogenesis. Additionally, we discuss the promise of dietary, probiotic, and pharmacological interventions in restoring the host's control over the IO microenvironment and microbiota, aiming to prevent and treat related diseases.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"100"},"PeriodicalIF":4.0,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12683929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707856","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}
Gut PathogensPub Date : 2025-12-08DOI: 10.1186/s13099-025-00767-4
Debora Compare, Bruno Fosso, Marcella Nunziato, Costantino Sgamato, Federica Di Maggio, Valeria D'Argenio, Ilaria Granata, Marco Sanduzzi Zamparelli, Domenica Lovero, Giorgio Casaburi, Alba Rocco, Pietro Coccoli, Graziano Pesole, Francesco Salvatore, Gerardo Nardone
{"title":"Gut mucosa-associated microbiota signatures in healthy individuals and patients at different stages of liver disease: a pilot study.","authors":"Debora Compare, Bruno Fosso, Marcella Nunziato, Costantino Sgamato, Federica Di Maggio, Valeria D'Argenio, Ilaria Granata, Marco Sanduzzi Zamparelli, Domenica Lovero, Giorgio Casaburi, Alba Rocco, Pietro Coccoli, Graziano Pesole, Francesco Salvatore, Gerardo Nardone","doi":"10.1186/s13099-025-00767-4","DOIUrl":"10.1186/s13099-025-00767-4","url":null,"abstract":"<p><strong>Background: </strong>The gut microbiota plays a key role in the progression of chronic liver disease and the development of hepatocellular carcinoma (HCC). However, findings on microbiota composition in such patients remain inconsistent, likely due to differences in disease aetiology and sample type. The mucosa-associated microbiota (MAM), residing in the intestinal mucin layer, more accurately reflects mucosal health than faecal microbiota, being more stable and less influenced by diet. This study aimed to characterise the ileal and sigmoid MAM in patients with chronic hepatitis C (CHC), liver cirrhosis (LC), and HCC.</p><p><strong>Methods: </strong>We performed DNA metabarcoding sequencing of mucosa samples collected from the ileum and sigmoid colon of patients at different stages of liver disease and healthy controls (HC). The predicted functions were analysed via phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) to infer metabolic pathways that can be expressed in the microbiome.</p><p><strong>Results: </strong>Among 33 participants (20 HCV-related liver disease and 13 healthy controls), MAM α-diversity decreased significantly in advanced disease stages, particularly in LC and HCC, regardless of the metric applied (p ≤ 0.05). β-diversity analyses showed distinct microbial community structures across groups. Both ileal and sigmoid MAM were dominated by Bacteroidetes, Firmicutes, and Proteobacteria, with enrichment of Firmicutes_D, Proteobacteria, and Fusobacteria in LC and HCC. Several genera, including Bulleidia, Pantoea, Clostridium_Q, Rothia, and Streptococcus, were significantly increased in HCC, whereas beneficial taxa such as Akkermansia and Butyricimonas were depleted. Functional predictions indicated enrichment of degradative pathways (e.g., taurine, chitin derivatives, and carbohydrate metabolism) in LC and HCC.</p><p><strong>Conclusion: </strong>Our pilot study suggests that MAM alterations do not directly mirror liver disease progression but show distinct patterns associated with different stages. These associations, more evident in advanced disease, involve bacterial taxa linked to gut integrity, inflammation, and carcinogenesis. This exploratory work lays the groundwork for future studies to validate these findings and investigate their relevance to microbiome-based diagnostics and therapies in HCC.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"99"},"PeriodicalIF":4.0,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12683826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707791","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}
Gut PathogensPub Date : 2025-12-07DOI: 10.1186/s13099-025-00774-5
Nasser Mousa, Alaa Elmetwalli, Mostafa Abdelsalam, Mohamed Wahba, Mohamed Selim, Dina Nour, Eman Abdelkader, Ahmed El-Eraky, Amany Hasson, Ahmed E Taha, Eman Mousa, Adel El-Assmy, Ali El-Assmy, Sherif Shiha, Muhammad Diasty, Mohammed Abdelaziz, Shereen A Mourad, Nader Elmalky, Marwa Mansour
{"title":"Risk stratification of spontaneous bacterial peritonitis recurrence: integrating acute kidney injury, biomarkers, composite scores, and machine learning models.","authors":"Nasser Mousa, Alaa Elmetwalli, Mostafa Abdelsalam, Mohamed Wahba, Mohamed Selim, Dina Nour, Eman Abdelkader, Ahmed El-Eraky, Amany Hasson, Ahmed E Taha, Eman Mousa, Adel El-Assmy, Ali El-Assmy, Sherif Shiha, Muhammad Diasty, Mohammed Abdelaziz, Shereen A Mourad, Nader Elmalky, Marwa Mansour","doi":"10.1186/s13099-025-00774-5","DOIUrl":"10.1186/s13099-025-00774-5","url":null,"abstract":"<p><strong>Background and aim: </strong>Recurrent spontaneous bacterial peritonitis (SBP) is a major concern for cirrhotic patients with ascites. This study seeks to identify predictors of recurrent SBP using clinical factors, inflammatory markers, and machine learning models.</p><p><strong>Patients and methods: </strong>The study involved 347 patients with cirrhotic ascites and SBP. Receiver Operating Characteristic (ROC) curve analysis assessed the predictive ability of biomarkers. A composite score was created to evaluate the risk stratification model. Different machine learning models were compared for predictive accuracy.</p><p><strong>Results: </strong>Eighty-three patients (23.9%) experienced recurrent SBP. Independent predictors of recurrence in multivariable analysis included acute kidney injury (AKI), elevated C-reactive protein (CRP) levels, higher serum bilirubin levels, a higher model for end-stage liver disease (MELD) score, proton-pump inhibitor (PPI) use, and lack of β-blocker use. A composite 10-point score (including AKI, CRP > 50 mg/L, low albumin levels < 2.5 g/dL, ascitic protein < 1.0 g/dL, albumin/ascitic ratio < 2.5 [2 points], MELD ≥ 15, diabetes, multidrug-resistant organism [MDRO] infection, and non-use of β-blockers) stratified the risk of recurrence into low (0-3: 15%), moderate (4-6: 45%), and high (7-10: 80%) categories. Machine learning models outperformed supervised machine logistic regression in predicting recurrence. Logistic regression achieved 70% accuracy, 65% sensitivity, and 68% specificity. The decision tree model improved accuracy to 75%, sensitivity to 72%, and specificity to 71%. The random forest model showed the best performance with 78% accuracy, 77% sensitivity, and 76% specificity.</p><p><strong>Conclusion: </strong>A composite score, combined with machine-learning models like random forest, enhances risk assessment for SBP recurrence. Clinical predictors such as AKI, CRP, bilirubin, MELD, PPI use, and β-blockers non-use help in targeted prevention.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":"103"},"PeriodicalIF":4.0,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12699928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696197","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}
Gut PathogensPub Date : 2025-12-06DOI: 10.1186/s13099-025-00779-0
Shafiul Haque, Abdulhadi I Bima, Ahmad O Babalghith, Naif A Jalal, Abdullah F Aldairi, Mohd Wahid, Faraz Ahmad, Farkad Bantun
{"title":"Distinct gut microbiota signatures and metabolic dysregulation in individuals with type 1 diabetes: insights into a microbiome-metabolite axis.","authors":"Shafiul Haque, Abdulhadi I Bima, Ahmad O Babalghith, Naif A Jalal, Abdullah F Aldairi, Mohd Wahid, Faraz Ahmad, Farkad Bantun","doi":"10.1186/s13099-025-00779-0","DOIUrl":"10.1186/s13099-025-00779-0","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence suggests a pivotal role for gut microbiota in the pathogenesis of Type 1 Diabetes (T1D). However, the compositional and functional characteristics of microbial dysbiosis in T1D remain incompletely understood. This study aimed to comprehensively characterize gut microbial alterations and associated metabolic shifts in individuals with T1D.</p><p><strong>Methods: </strong>The present study is based on re-analysis of publicly available 16S rRNA sequencing and fecal untargeted metabolomics data from T1D patients and healthy controls generated by Yuan et al. (2022, Nature Communications). Microbial diversity was assessed using Chao1 and Fisher indices (alpha diversity), and Bray-Curtis-based Principal Coordinates Analysis (PCoA) (beta diversity). Taxonomic differences were examined at phylum, genus, and species levels, and differentially abundant taxa were identified via Linear Discriminant Analysis Effect Size (LEfSe). Correlation analyses were conducted to explore microbe-metabolite interactions.</p><p><strong>Results: </strong>T1D individuals exhibited reduced alpha diversity and distinct beta diversity clustering compared to controls, indicating substantial shifts in microbial richness and community structure. Taxonomic analysis revealed an increased abundance of Escherichia-Shigella, Veillonella atypica, and Erysipeloclostridium ramosum in T1D, and depletion of beneficial taxa such as Bifidobacterium, Parabacteroides distasonis, Alistipes putredinis, and Bacteroides plebeius. LEfSe analysis confirmed these patterns and highlighted a T1D-specific microbial signature. Integrative correlation analysis uncovered functional dysbiosis, wherein depleted commensals were positively associated with anti-inflammatory and bioenergetic metabolites (e.g., D-gluconic acid, lactic acid, pyruvate), while T1D-enriched taxa were linked to metabolites involved in oxidative stress and immune activation.</p><p><strong>Conclusion: </strong>Our study reveals profound structural and functional alterations in the gut microbiome of individuals with T1D. These findings support the existence of a gut microbial-metabolite axis in autoimmune diabetes and suggest that microbial biomarkers and metabolic pathways may serve as novel targets for early diagnosis and therapeutic intervention. Longitudinal studies are warranted to validate these signatures and explore microbiota-based therapies for T1D prevention and management.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":"98"},"PeriodicalIF":4.0,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12683924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696212","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}
Gut PathogensPub Date : 2025-12-03DOI: 10.1186/s13099-025-00778-1
Omar Noman, Nicole Tegtmeyer, Bodo Linz, Mathias Müsken, Steffen Backert
{"title":"Extracts from Plectranthus asirensis and Premna resinosa inhibit Helicobacter pylori-induced epithelial cell damage, DNA double-strand breaks and inflammation.","authors":"Omar Noman, Nicole Tegtmeyer, Bodo Linz, Mathias Müsken, Steffen Backert","doi":"10.1186/s13099-025-00778-1","DOIUrl":"10.1186/s13099-025-00778-1","url":null,"abstract":"<p><strong>Background: </strong>Helicobacter pylori infection is a major global health issue associated with chronic gastritis, peptic ulcers, and gastric cancer. Due to the increasing resistance of H. pylori to conventional antibiotics, there is growing interest in researching alternative therapeutic agents, particularly those from medicinal plants.</p><p><strong>Methods: </strong>Preparation and purification of extracts from two plant species, Plectranthus asirensis and Premna resinosa, were performed by cold maceration. The anti-microbial activity of two extracts was then evaluated against H. pylori to determine the minimum inhibitory concentration (MIC). The activity of the extracts was further analyzed by electron microscopy, bacterial cell lysis and Western blotting. The effects on AGS gastric epithelial cells upon infection were monitored by cell scattering, cell vacuolization, DNA damage analysis, NF-κB reporter assay and chemokine ELISA.</p><p><strong>Results: </strong>We determined the MIC of P. asirensis and P. resinosa extracts on treated H. pylori as 200 µg/mL and 35 µg/mL, respectively. Electron microscopy showed severe deformation of the bacterial cells. We obtained no bacterial cell lysis and only minimal changes in protein expression levels of the virulence factors CagA, CagY, HopQ, urease, and flagellin. However, we found that cleavage of the vacuolating cytotoxin VacA p98 pro-form to the p88 active form was significantly downregulated. The enzymatic urease activity was also impaired by the addition of both extracts, while the proteolytic activity of serine protease HtrA was not affected. Infection of AGS cells in the presence of both extracts revealed that type IV secretion system (T4SS)-dependent CagA injection, cell scattering and motility, as well as VacA-dependent cellular vacuolation were completely inhibited. Furthermore, H. pylori-induced pro-inflammatory transcription factor NF-κB and interleukin-8 release were also significantly downregulated. Finally, both extracts prevented T4SS-induced DNA double-strand breaks (DSBs) and chromosomal fragmentation in the nuclei of host cells.</p><p><strong>Conclusions: </strong>Taken together, we have discovered natural compounds of P. asirensis and P. resinosa that exhibit potent anti-H. pylori activities, not only inhibiting bacterial growth, but also suppressing key virulence mechanisms involved in epithelial cell damage, inflammation and genomic instability. These extracts are promising candidates for future therapeutic applications in patients, which could help minimizing H. pylori infections and gastric cancer development.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"97"},"PeriodicalIF":4.0,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660954","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}
Gut PathogensPub Date : 2025-12-02DOI: 10.1186/s13099-025-00780-7
Chun-Ting Chen, Annemiek A van der Eijk, Jolanda J C Voermans, Hanneke J van Vuuren, Maikel P Peppelenbosch, Vincent T Janmaat
{"title":"Nasopharyngeal viral infection as a source of elevated fecal calprotectin: a diagnostic pitfall in intestinal inflammation.","authors":"Chun-Ting Chen, Annemiek A van der Eijk, Jolanda J C Voermans, Hanneke J van Vuuren, Maikel P Peppelenbosch, Vincent T Janmaat","doi":"10.1186/s13099-025-00780-7","DOIUrl":"10.1186/s13099-025-00780-7","url":null,"abstract":"<p><p>Fecal calprotectin is widely used as a non-invasive biomarker for intestinal inflammation, particularly in inflammatory bowel disease (IBD), the most common clinical context for its use, where misinterpretation can lead to unnecessary invasive procedures or inappropriate therapy escalation. However, its specificity has been questioned due to elevated levels observed in non-intestinal conditions. Here, we investigated whether nasopharyngeal viral infections contribute to elevated fecal calprotectin, thereby confounding its diagnostic interpretation. Bioinformatic analysis revealed high constitutive expression of calprotectin subunits (S100A8/A9) in squamous epithelia of the upper aerodigestive tract compared with distal gut mucosa. To assess gastrointestinal stability of epithelial-derived calprotectin, healthy volunteers ingested porcine calprotectin, which was subsequently detected in feces, demonstrating resistance to intestinal degradation. In a retrospective cohort, patients with non-SARS-CoV-2 respiratory viral infections displayed significantly higher fecal calprotectin levels than SARS-CoV-2 patients (447 µg/g vs. 82 µg/g, p < 0.001), despite limited gastrointestinal involvement. Nasopharyngeal calprotectin levels did not differ significantly between viral etiologies, but in COVID-19 patients, fecal calprotectin positively correlated with nasopharyngeal calprotectin (R = 0.43, p = 0.008) and viral load (R = 0.13, p = 0.026). These findings suggest that calprotectin released from proximal epithelial tissues during viral infection can persist through the gastrointestinal tract and influence fecal calprotectin levels, underscoring the importance of contextual interpretation of this biomarker and the value of incorporating virological assessment into diagnostic workflows.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"95"},"PeriodicalIF":4.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660966","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}
Gut PathogensPub Date : 2025-12-02DOI: 10.1186/s13099-025-00771-8
Monique Pinto-Gonçalves, Beatriz Iandra da Silva Ferreira, Alda Maria Da-Cruz, Otacílio da Cruz Moreira, Maria Fantinatti
{"title":"High resolution melting real-time PCR for genotyping of Giardia lamblia assemblages A and B regardless of parasite load.","authors":"Monique Pinto-Gonçalves, Beatriz Iandra da Silva Ferreira, Alda Maria Da-Cruz, Otacílio da Cruz Moreira, Maria Fantinatti","doi":"10.1186/s13099-025-00771-8","DOIUrl":"10.1186/s13099-025-00771-8","url":null,"abstract":"<p><p>Giardia lamblia is a globally distributed fecal-oral transmitted enteroparasite. G. lamblia is phylogenetically divided into assemblages A to H. Assemblages A and B have high zoonotic potential, as reported in humans and other animals, including dogs and cats. Currently, G. lamblia genotyping is performed using gene sequencing, which is an expensive technique, especially in developing countries where higher frequencies of the protozoan have been reported. Real-time PCR with High Resolution Melting (qPCR-HRM) is a sensitive method for detecting polymorphisms and is used for differentiate species, subspecies, and assemblages. This study aimed to standardize and validate the qPCR-HRM technique for genotyping G. lamblia in human fecal samples, regardless of the parasite load. qPCR-HRM was standardized using the β-giardin target, and validation was performed using DNA extracted from fecal samples (n = 76). Sanger sequencing of the same genetic target was used the gold standard. Genotyping of the samples (assemblages A and B) was performed using both techniques, and qPCR-HRM demonstrated 98.08% concordance with the sequencing results. Only one sample showed a discrepancy in the assemblage determination between the techniques. DNA sequencing failed to characterize 24 samples from patients with low or moderate parasite loads. Thus, qPCR-HRM successfully differentiate 23 samples into assemblage A and one as assemblage B. In this context, when compared to sequencing, the qPCR-HRM technique proved to be effective for genotyping G. lamblia, even in samples with a low parasite load, with the potential to significantly reduce execution time and financial investment required to identify G. lamblia assemblages. This tool can be strategic for strengthening public health policies for the surveillance and control of giardiasis.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"96"},"PeriodicalIF":4.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660995","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":"CagA-positive H. pylori may protect against disease of the hands, feet, and mouth.","authors":"Qiuying Du, Weifeng Wang, Fenglian Deng, Jianyu Cao, Xiaoxian Wei, Zengjing Liu, Chunyi Long, Jing Pan, Liudan Liang, Guangfu Pang, Yuefeng Huang, Shengkui Tan, Jiannan Lv","doi":"10.1186/s13099-025-00763-8","DOIUrl":"10.1186/s13099-025-00763-8","url":null,"abstract":"<p><strong>Background: </strong>The incidence of an infection with Helicobacter pylori, or H. pylori rises with age, mostly affecting children.The infection rate of Helicobacter pylori increases with age, primarily affecting children. The rate of cases of disease of the hands, feet, and mouth (HFMD), an infectious illness that mostly affects newborns and young children and is ubiquitous throughout the Asia-Pacific area, declines with age. Asthma, shigellosis, TB, anaphylactic disease, and other diarrheal illnesses are all prevented by H. pylori. It also has a strong correlation with infectious disorders brought on by infection with pathogens including Orientia tsutsugamushi, HIV, HCV, and Brucella abortus. Nonetheless, the status of infection with H. pylori in individuals already infected with HFMD and the clinical implications of CagA<sup>+</sup> H. pylori strains remain unreported.</p><p><strong>Methods: </strong>From October 2020 to October 2023, 130 children clinically diagnosed with HFMD enrolled in the observation group at the Affiliated Hospital of Youjiang Medical University for Nationalities Affiliated Hospital of Youjiang Medical College of Nationalities and the People's Hospital of Beihai. With respect to gender, age, and location of residence, 150 chronologically matched healthy children made up the control group. Serum H. pylori antibodies in patients were measured, and the strain was identified through the Western blot technique.</p><p><strong>Results: </strong>1. The frequency of infections with H. pylori with the prevalence of CagA + strains were found to be 16.2% and 8.5%, respectively, in patients with HFMD. These figures are lower than the 29.3% and 18.0% that are seen in healthy children, respectively (P-value < 0.05 for both). 2. The infection rate of the bacteria H. pylori and CagA + strains was found to be 18.5% and 9.3% in HFMD patients over 5 years of age, which is lower than the 41.5% and 26.2% observed in healthy children over 5 years, respectively (P-value < 0.05). In contrast, the rate of H. pylori and CagA + strains in HFMD patients aged 5 years and below was comparable to that of healthy children in the same age group, with both results showing no statistically significant differences. 3. H. pylori and CagA + strain prevalence were similar in primary and subsequent HFMV infections, although neither was statistically significant. 4.The findings of the univariate and multivariate analyses indicated that vaccination against HFMD and infection with H. pylori CagA + were protective factors against HFMD (0.203; 0.069-0.593; 0.004).</p><p><strong>Conclusion: </strong>When compared to children in good health, individuals with HFMD had much lower levels of Helicobacter pylori infection. Additionally, H. pylori that carries the CagA gene could be able to prevent the development of HFMD.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"93"},"PeriodicalIF":4.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12642171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145587210","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}
Gut PathogensPub Date : 2025-11-23DOI: 10.1186/s13099-025-00786-1
Tingting Ning, Nianchen Liu, Qi Jiang, Nan Zhang, Shengtao Zhu
{"title":"Patients with inflammatory bowel disease exhibit increased susceptibility to HCoV-NL63.","authors":"Tingting Ning, Nianchen Liu, Qi Jiang, Nan Zhang, Shengtao Zhu","doi":"10.1186/s13099-025-00786-1","DOIUrl":"10.1186/s13099-025-00786-1","url":null,"abstract":"<p><p>Immunocompromised inflammatory bowel disease (IBD) patients may develop life-threatening pneumonia and bronchiolitis upon HCoV-NL63 infection. However, little is known whether these patients will be more susceptible to HCoV-NL63 infection. We compared the expression of ACE2 in different tissues and cell lines. Besides, the susceptibility of colonic cells to HCoV-NL63 was assessed. We then examined the expression of ACE2 in the colonic mucosa from IBD patients and animal models, and in the inflammatory colonic cells. The susceptibility of inflammatory colonic cells to HCoV-NL63 was detected using a pseudovirus-based system. Pseudovirus based neutralization assay was used to quantify the neutralizing antibodies to HCoV-NL63 in patients with IBD and healthy controls. ACE2 was abundantly expressed in the colonic tissue and cells. And colonic cells were susceptible to pseudotyped HCoV-NL63. The expression of ACE2 was increased in the colonic mucosa from IBD patients and animal models, and in inflammatory colonic cells. Inflammatory colonic cells were more susceptible to pseudotyped HCoV-NL63. Besides, reduced protective neutralizing antibody titers were seen in patients with IBD, especially for male or older IBD patients. These results suggest IBD patients may be particularly susceptible to infection with HCoV-NL63 and thus extra precautions should be taken to prevent them from infection. Further mechanistic studies are needed to support our findings.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":" ","pages":"101"},"PeriodicalIF":4.0,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12683868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145587215","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}
Gut PathogensPub Date : 2025-11-20DOI: 10.1186/s13099-025-00775-4
Xueyan Gao, Feiyu Cao, Yonghao Li, Jingjie Huang, Xuan Hu, Ziyun Li
{"title":"Fusobacterium nucleatum: a transboundary pathogen in host-microbiota networks.","authors":"Xueyan Gao, Feiyu Cao, Yonghao Li, Jingjie Huang, Xuan Hu, Ziyun Li","doi":"10.1186/s13099-025-00775-4","DOIUrl":"10.1186/s13099-025-00775-4","url":null,"abstract":"<p><p>Fusobacterium nucleatum (Fn), a gram-negative anaerobic bacterium,, transitions from oral commensal to systemic pathogen in colorectal cancer (CRC), inflammatory bowel disease (IBD), arthritis, and preterm birth. This review synthesizes Fn's subspecies-specific pathogenic mechanisms. Its virulence factors enable immune evasion, inflammation modulation, and tumor progression. In the gastrointestinal tract, Fn disrupts intestinal barrier integrity through paracellular and apoptotic pathways, activates Th17/ T regulatory (Treg) immune balance alterations, and induces macrophage polarization. Moreover, Fn's role in tumorigenesis involves biofilm formation and metabolic regulation. Within microbial networks, Fn exhibits both synergistic and antagonistic interactions. It collaborates with pathogens like Clostridioides difficile and Pseudomonas aeruginosa to enhance infection, while being inhibited by probiotics such as Lactobacillus rhamnosus and Akkermansia muciniphila. Notably, microbial metabolites like butyrate and hydrogen sulfide display context-dependent roles-some may drive disease progression, while others may suppress it. This comprehensive review highlights Fn's pathogenicity and its complex interactions within microbial communities, offering novel interventions for microbiota-driven pathologies.</p>","PeriodicalId":12833,"journal":{"name":"Gut Pathogens","volume":"17 1","pages":"92"},"PeriodicalIF":4.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12632115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556756","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}