Gastroenterology最新文献

{"title":"Irritable bowel syndrome and suicide risk","authors":"Mohamed G. Shiha, Imran Aziz","doi":"10.1053/j.gastro.2026.10.377","DOIUrl":"https://doi.org/10.1053/j.gastro.2026.10.377","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":"5 1","pages":""},"PeriodicalIF":29.4,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149236191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Building a Better Model for Fecal Calprotectin Monitoring in Inflammatory Bowel Disease: Room for Some Home Improvement.","authors":"David T Rubin","doi":"10.1053/j.gastro.2026.10.004","DOIUrl":"10.1053/j.gastro.2026.10.004","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk-Adapted Endoscopic Follow-Up After Achalasia: A Clinical Consideration.","authors":"Chuang Yan, Kangyu Liu, Gong Zhang","doi":"10.1053/j.gastro.2026.04.050","DOIUrl":"10.1053/j.gastro.2026.04.050","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply.","authors":"Wilhelm Leijonmarck, Jesper Lagergren","doi":"10.1053/j.gastro.2026.10.002","DOIUrl":"10.1053/j.gastro.2026.10.002","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Temperature Protein G-High-Expressing Escherichia coli Promotes Fibrosis in Chronic Pancreatitis.","authors":"Li-Long Pan, Wenjie Liang, Zhengnan Ren, Jun Yang, Kunpeng Jia, Qiwen Wang, Yu Ma, Haizhi Tian, Huimin Zou, He Liu, Lili Wang, Meirong Wu, Binbin Li, Siqi Yang, Jihui Zuo, Zhuo Wang, Qiuyang Yang, Xiaoliang Dong, Madhav Bhatia, Shuang Peng, Chunhua Zhou, Wen-Bin Zou, Zhuan Liao, Duowu Zou, Julien Diana, Jia Sun","doi":"10.1053/j.gastro.2026.09.025","DOIUrl":"10.1053/j.gastro.2026.09.025","url":null,"abstract":"<p><strong>Background & aims: </strong>Chronic pancreatitis (CP) is a progressive fibroinflammatory disease with increasing global incidence and no curative therapy. Gut dysbiosis has been associated with CP, but its causal contribution to disease pathogenesis remains unclear. We intended to identify specific pathogenic microbial species that promote CP and to delineate the underlying pathogenic mechanisms.</p><p><strong>Methods: </strong>Multiomics analyses were used to identify key microbial signatures in CP patients and mice. Novel pathogenic Escherichia coli strains were isolated and bioengineered for functional studies. In vitro and in vivo assays, along with macrophage-specific knockout mice, adenoviral tools, and pharmacologic inhibitors, were used to dissect host-microbe mechanistic pathways. Therapeutic intervention included administering a screened next-generation probiotic.</p><p><strong>Results: </strong>Metagenomic sequencing identified high-temperature protein G (HtpG)-high-expressing E coli (HHEC) enrichment as a dominant microbial signature in CP patients. Prevention of HHEC adherence and colonization alleviated CP, whereas recolonization with a new patient-derived HHEC strain PS718 exacerbated it. Mechanistically, E coli-derived HtpG up-regulated protein arginine methyltransferase 5 (PRMT5) in pancreatic macrophages. Pharmacologic inhibition of PRMT5 or macrophage-specific deletion of PRMT5 mitigated pancreatic fibrosis and CP progression. PRMT5 methylated Krüppel-like factor 4 at residues R387/R389, stabilizing it, which promoted M2 polarization and pancreatic fibrosis. Therapeutic intervention with Akkermansia muciniphila, which is reduced in CP, suppressed HHEC colonization and ameliorated CP.</p><p><strong>Conclusions: </strong>These findings provide novel evidence for a pathogenic HHEC-HtpG-macrophage axis in CP, highlighting the potential of microbiota-targeted therapies for the condition.</p>","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myofibroblast-Derived Transglutaminase 2 Activity is Upregulated in Stricturing Crohn's Disease and Its Inhibition Exerts Antifibrotic Properties.","authors":"Jyotsna Chandra, Doug Czarnecki, Pranab K Mukherjee, Gail A West, Ilyssa O Gordon, Thomas Plesec, Yan Wang, Sinan Lin, Jie Wang, Marianne Bergin, Linghong Huang, Ren Mao, Nguyen Quang Tam, Weiwei Liu, William J Massey, Suhanti Banerjee, Ankita Prasad, Andrei I Ivanov, Samantha Gauriloff, Mark E Baker, Joseph Sleiman, Katherine Falloon, Claire A Beveridge, Catherine Larsen, Sean Kessler, Olga Lavryk, Jeremy Lipman, Stefan Holubar, Shaomin Hu, Claudio Fiocchi, Timothy Johnson, Carol de la Motte, Florian Rieder","doi":"10.1053/j.gastro.2026.09.026","DOIUrl":"10.1053/j.gastro.2026.09.026","url":null,"abstract":"<p><strong>Background & aims: </strong>Excessive accumulation of extracellular matrix (ECM) derived from human intestinal myofibroblasts (HIMFs) drives the significant clinical problem of intestinal fibrosis. Fibrosis is believed to progress even in the absence of intestinal inflammation. The ECM-bound transglutaminase 2 (TG2) enzyme may exert direct profibrotic effects. We investigated the role of TG2 in intestinal fibrosis.</p><p><strong>Methods: </strong>TG2 expression and activity in human intestinal tissue and HIMFs from patients with strictured Crohn's disease and control subjects were measured. ECM accumulation by HIMF in the presence or absence of TG2 inhibitors was determined. Putative TG2 signaling pathways discovered in HIMF using bulk RNA sequencing and single-cell RNA sequencing were functionally validated. Role of TG2 in vivo was confirmed using inducible global knockout of TGM2 (encoding TG2) in 2 experimental fibrosis models.</p><p><strong>Results: </strong>Transglutaminase (TG) activity was increased in strictured Crohn's disease compared with controls, with up to 100% activity attributable to TG2. TG activity correlated with the degree of histopathologic tissue fibrosis. HIMFs were the major source of TG2, with ≥95% of HIMF TG activity being derived from TG2. Tissue distribution of TG2 in myofibroblasts was confirmed by single-cell RNA sequencing. Selective inhibition of TG2 activity reduced fibronectin and collagen I, III, and VI accumulation by HIMFs. Novel TG2 signaling pathways revealed by bulk RNA sequencing were functionally validated. Inducible TGM2 knockout prevented experimental fibrosis without affecting the degree of intestinal inflammation.</p><p><strong>Conclusions: </strong>TG2 may be involved in inflammation-independent progression of intestinal fibrosis.</p>","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"History of Childhood Abuse Is Associated With Chronic Constipation Decades Later in Adulthood.","authors":"Peenaprapa Tangpradubkiat, Andrea L Roberts, Yiqing Wang, Kai Wang, Kyle Staller, Andrew T Chan","doi":"10.1053/j.gastro.2026.09.022","DOIUrl":"10.1053/j.gastro.2026.09.022","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HLA-DRB1∗01:03 Is a Reproducible Biomarker of Colectomy Risk in Ulcerative Colitis.","authors":"Kelly C Cushing-Damm, Lishi Yin, Yanhua Chen, Antonino Oliveri, Peter D R Higgins, Elizabeth K Speliotes","doi":"10.1053/j.gastro.2026.09.017","DOIUrl":"10.1053/j.gastro.2026.09.017","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut Inflammation Favors Adverse Food Reactions by Disrupting the Microbial Metabolism of Food Triggers.","authors":"Bruna B Da Luz, Liam E Rondeau, Rebecca Dang, Dana Coppens, Dominika Boron, Pranshu Muppidi, Anastasia Christoforou, Jessica Linton, Fernando A Vicentini, John K Marshall, Giada De Palma, Premysl Bercik, Neeraj Narula, Alberto Caminero","doi":"10.1053/j.gastro.2026.07.042","DOIUrl":"10.1053/j.gastro.2026.07.042","url":null,"abstract":"<p><strong>Background & aims: </strong>Food-related adverse reactions are frequently reported by patients with inflammatory bowel disease (IBD), but the underlying mechanisms are poorly understood. We investigated how intestinal inflammation and the microbiota contribute to the development of adverse food reactions.</p><p><strong>Methods: </strong>We sensitized mice to different foods (dairy and gluten) after intestinal inflammation (chemically and hapten-induced models), then mice were re-exposed to the sensitizing foods through diet enrichment. To study whether inflamed microbiota facilitates adverse food reactions, we used gnotobiotic models and bacterial supplementation experiments. We assessed markers of intestinal inflammation and sensitization, clinical responses, RNA transcripts, and microbiota composition and function. In a translational approach, we recruited IBD patients in remission and healthy controls, recorded self-reported food intolerances and clinical responses to triggering foods, and collected feces for gut microbiota analyses.</p><p><strong>Results: </strong>Intestinal inflammation facilitates food sensitization by disrupting microbial antigen metabolism, recruiting mast cells to the colon, and favoring immunoglobulin E production. In gnotobiotic models, inflammation-driven depletion of colonic bacteria involved in food digestion contributed to food sensitization. Upon re-exposure to triggering foods, sensitized mice experienced visceral pain and low-grade inflammation through mast cell-mediated mechanisms, which also worsened experimental colitis. Supplementation with depleted bacteria or treatment with mast cell stabilizers attenuated food-driven responses. In IBD patients, self-reported food intolerances were common and associated with microbial disruption and depletion of food-metabolizing bacteria.</p><p><strong>Conclusions: </strong>Microbial metabolism of foods is disrupted after intestinal inflammation. This facilitates food sensitization, through colonic mast cell-mediated immune responses, which may explain the high number of adverse food reactions reported by IBD patients.</p>","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":" ","pages":""},"PeriodicalIF":29.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer risks for first-degree relatives of people with double somatic DNA mismatch repair mutations","authors":"Romy Walker,James G. Dowty,Rachel Pearlman,Alicia Latham,Mark Clendenning,Sharelle Joseland,Hsin-Lun Liao,Peter Georgeson,Julia Como,Jihoon E. Joo,Khalid Mahmood,Bernard J. Pope,Fiona Phillips,Christophe Rosty,Finlay A. Macrae,Ingrid M. Winship,Aung K. Win,Amanda I. Phipps,Steven Gallinger,Robert C. Grant,John D. Potter,N. Jewel Samadder,Susan Parry,Julie Arnold,Varnika Vijay,Ahmed Bouras,Cédrick Lefol,Qing Wang,Aliya Khurram,Yelena M. Kemel,Mohammad Ali Abbass,Sara H.M. Keshavjee,Zsofia K. Stadler,Heather Hampel,Mark A. Jenkins,Daniel D. Buchanan","doi":"10.1053/j.gastro.2026.09.015","DOIUrl":"https://doi.org/10.1053/j.gastro.2026.09.015","url":null,"abstract":"","PeriodicalId":12590,"journal":{"name":"Gastroenterology","volume":"24 1","pages":""},"PeriodicalIF":29.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}