Journal of Gastroenterology最新文献

{"title":"Gut microbiome-enteric virus interactions: mechanisms, clinical implications, and translational directions.","authors":"Anoushka Saxena, Maryam Javed, Nirupama Trehanpati","doi":"10.1007/s00535-026-02524-z","DOIUrl":"https://doi.org/10.1007/s00535-026-02524-z","url":null,"abstract":"<p><p>The gut microbiome influences epithelial barrier integrity, metabolite availability, mucosal immune tone, and vaccine responsiveness, all of which are relevant to enterically transmitted viral infection. Norovirus and rotavirus primarily replicate in the intestinal mucosa and cause acute gastroenteritis, whereas poliovirus replicates in the gut and may disseminate systemically. Hepatitis A virus and hepatitis E virus are acquired through the intestine and shed fecally, but their dominant clinical manifestation is hepatitis. This review synthesizes evidence linking the bacteriome, phageome/virome, and mycobiome with these viruses, while explicitly distinguishing direct enteric virus mechanisms from broader microbiome-immune or metabolite pathways and from cross-kingdom evidence extrapolated from intestinal inflammation or pathobiont studies. The strongest evidence supports selected virus-bacterium and virus-metabolite mechanisms, including bacterial glycan interactions in norovirus, bacterial LPS-mediated poliovirus stabilization, bile acid-dependent human norovirus replication in enteroids, and rotavirus-associated barrier disruption. Human studies remain dominated by stool-based associations that are difficult to separate from inflammation, diet, antibiotic exposure, diarrhea, and sampling time. We therefore rank evidence across experimental, organoid, animal, human observational, and clinical-translational levels, and highlight concrete applications for severe gastroenteritis risk prediction, prolonged shedding, impaired barrier recovery, and oral vaccine nonresponse. Future progress will require longitudinal, spatially resolved, multi-kingdom, and multi-omics studies linked to human-relevant experimental systems.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthcare burden and clinical spectrum of symptomatic polycystic liver disease in Japan: a nationwide epidemiological survey.","authors":"Kota Tsuruya, Satoko Ohfuji, Tatsuya Suwabe, Yusuke Mishima, Yoshitaka Arase, Shunji Hirose, Satsuki Ieda, Junichi Hoshino, Shintaro Yagi, Kiyoshi Hasegawa, Atsushi Tanaka, Tatehiro Kagawa","doi":"10.1007/s00535-026-02522-1","DOIUrl":"https://doi.org/10.1007/s00535-026-02522-1","url":null,"abstract":"<p><strong>Background: </strong>Polycystic liver disease (PLD) is often asymptomatic, but some patients develop symptoms or complications requiring care or intervention. The nationwide burden of symptomatic PLD remains poorly defined. We conducted a nationwide survey to estimate the number and prevalence of patients with symptomatic PLD in Japan and characterize clinical features, treatment patterns, healthcare utilization, and outcomes.</p><p><strong>Methods: </strong>A nationwide two-stage questionnaire survey was conducted. Symptomatic PLD was defined as 10 or more hepatic cysts with cyst-related symptoms or complications. In the first-stage survey, 3127 departments were selected by stratified random sampling to estimate the number of patients treated or followed up during 2021-2023. In the second-stage survey, clinical data were collected for patients treated or followed up in 2023.</p><p><strong>Results: </strong>The estimated number of patients was 6500 during 2021-2023 and 3570 in 2023, corresponding to an annual prevalence of 28.6 per million. Among 557 patients with clinical data, 62% were female and 67.2% met the diagnostic criteria for polycystic kidney disease. Abdominal distension, abdominal pain, and cyst infection were the most frequent manifestations. More than half underwent hepatic cyst treatment, and 60.4% required consultation with other departments or institutions. Cyst infection and liver failure accounted for a subset of deaths. Mortality differed significantly among Gigot classification groups and was highest in type III.</p><p><strong>Conclusions: </strong>This nationwide survey provides the first comprehensive epidemiological and clinical characterization of symptomatic PLD in Japan and establishes a benchmark for future disease severity classification, clinical management, and prospective studies.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Genome-scale activation screen reveals lncRNA HNF1A-AS1 promotes pancreatic cancer metastasis through interacting with U2SURP to increase CD44 alternative splicing.","authors":"Shan Lei, Zhixue Zhang, Zhirui Zeng, Wenpeng Cao, Yating Sun, Dahuan Li, Jigang Pan, Yingmin Wu, Tuo Zhang, Tengxiang Chen","doi":"10.1007/s00535-026-02521-2","DOIUrl":"https://doi.org/10.1007/s00535-026-02521-2","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S-adenosylhomocysteine hydrolase-like protein 1 deficiency resulted in stronger inflammation reaction in acute pancreatitis.","authors":"Juan Xiao, Wanlian Li, Jian Pan, Yinhui Yang, Ji-Ao Chen, Xi-Dai Long","doi":"10.1007/s00535-026-02437-x","DOIUrl":"10.1007/s00535-026-02437-x","url":null,"abstract":"<p><strong>Background: </strong>The mechanism underlying acute pancreatitis (AP) is not fully understood. And the effect of s-adenosylhomocysteine hydrolase-like protein 1 (AHCYL1) in AP is unknown.</p><p><strong>Methods: </strong>In this research, AHCYL1 pancreatic acinar cell specific knockout (CKO) mice were constructed and AP was induced. The related mechanism was investigated in mice or primary cells.</p><p><strong>Results: </strong>It was found that AHCYL1 was decreased in AP mice. CKO caused increased macrophage infiltration in AP pancreas. AHCYL1 binding to amino acid transporters decreased in AP. Amino acid uptake, mTOR inhibition, and MIF production were aggravated in AP with AHCYL1 deficiency. Differentially expressed PGK1 in proteomics was associated with both mTOR and MIF in the PPI network. PGK1 was found to be further increased in CKO AP pancreas, which was reversed by mTOR activator. MIF expression and secretion under AP were inhibited by mTOR activator or PGK1 inhibitor. MIF-induced macrophage migration could be reduced by mTOR activator or PGK1 inhibitor. N1-acetylspermine increased in the serum of CKO AP mice. CKO acinar cell culture under AP caused further increment in N1-acetylspermine production enzyme, SSAT, which was inhibited by mTOR activator or PGK1 inhibitor. MIF induced SSAT and cytokines from macrophages, and the latter was reduced by SSAT inhibitor. Finally, AHCYL1 binding to the deubiquitinase OTUD6B decreased in AP. OTUD6B knockdown caused AHCYL1 ubiquitination and its decrement. AHCYL1 recovery reduced cytokine release and macrophage infiltration in AP.</p><p><strong>Conclusion: </strong>The AHCYL1 deficiency/amino acid uptake inhibition/mTOR inhibition/PGK1 up-regulation/MIF secretion axis in acinar cells induced SSAT in macrophages and macrophage infiltration in the pancreas in AP.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1483-1501"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S1P receptor modulators for moderate-to-severe ulcerative colitis: a systematic review, meta-analysis, and trial sequential analysis.","authors":"Abdulkareem Jomaa, Rani Bshara, Mohammed Alani, Bilind Ismail, Yousif Rajab, Dani Hayder, Halder J Abozait, Wasim Jomaa, Weys Neda, Mostafa Najim, Hasan Al-Obaidi","doi":"10.1007/s00535-026-02485-3","DOIUrl":"10.1007/s00535-026-02485-3","url":null,"abstract":"<p><strong>Background and aims: </strong>S1P receptor modulators are emerging oral therapies for moderate-to-severe ulcerative colitis (UC); however, a comprehensive synthesis incorporating the largest number of RCTs to date, alongside Trial Sequential Analysis (TSA) and GRADE-based certainty assessment, remains lacking. We aim to evaluate the efficacy and safety of S1P receptor modulators in moderate-to-severe UC and assess the conclusiveness and certainty of the evidence.</p><p><strong>Methods: </strong>PubMed, Cochrane Library, Europe PMC, and Google Scholar were searched from inception through February 28, 2026. Eligible studies were RCTs comparing any S1P receptor modulator with placebo in adults (≥ 18 years) with UC. Pooled risk ratios (RRs) with 95% CIs were estimated using a random-effects model.</p><p><strong>Results: </strong>A total of ten RCTs were included. During induction, S1P receptor modulators were superior to placebo for clinical remission (RR 2.77; 95% CI, 2.17-3.55; I² = 0%), clinical response (RR 1.69, 95% CI 1.52-1.87; I² = 0%), endoscopic improvement (RR, 2.29; 95% CI, 1.91-2.75; I² = 0%), and histological remission (RR 2.77; 95% CI, 2.11-3.63; I² = 0%). Maintenance outcomes were similarly significant but heterogeneous (I² = 48%-65%), fully resolved when restricted to treat-through designs. SAEs were not increased, while TEAEs were modestly higher overall during combined induction and maintenance periods, mainly with etrasimod. TSA provided supportive evidence of conclusive superiority for clinical response at both induction and maintenance, and for endoscopic improvement at induction; evidence for other outcomes remained inconclusive. GRADE certainty of evidence was moderate to high across all efficacy outcomes.</p><p><strong>Conclusion: </strong>S1P receptor modulators demonstrated moderate-to-high certainty evidence of efficacy across all outcomes, without a significant increase in SAEs. These findings provide robust quantitative support for current guideline recommendations endorsing this oral drug class as an effective advanced therapy for moderate-to-severe UC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1382-1392"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to: comment on \"Validation of Baveno VII criteria for recompensation in patients with decompensated cirrhosis treated by laparoscopic splenectomy and azygoportal disconnection\".","authors":"Liu-Xin Zhou, Bao-Yu Wan, Hao Dong, A-Long Shi, Guoqing Jiang","doi":"10.1007/s00535-026-02497-z","DOIUrl":"10.1007/s00535-026-02497-z","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1522-1523"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"Validation of Baveno VII criteria for recompensation in patients with decompensated cirrhosis treated by laparoscopic splenectomy and azygoportal disconnection\".","authors":"Congcong Song, Zhongxiao Zhou, Xin Li","doi":"10.1007/s00535-026-02444-y","DOIUrl":"10.1007/s00535-026-02444-y","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1520-1521"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SEVs-carried ENPP1 regulates DCs' activation and inhibits the formation of tertiary lymphoid structures in gastric cancer.","authors":"Wenbo Liu, Bingyu Wang, Xinyu Yuan, Zhiran Yang, Yingying Wang, Zhiyuan Wang, Yong Li, Fang Li, Limian Er, Bibo Tan","doi":"10.1007/s00535-026-02459-5","DOIUrl":"10.1007/s00535-026-02459-5","url":null,"abstract":"<p><strong>Background: </strong>Ectonucleotide pyrophosphatase/phosphodiesterase 1(ENPP1) is a potential immune checkpoint, but the role and mechanism of small extracellular vesicles (sEVs)-carried ENPP1 in the formation of tertiary lymphoid structures (TLS) in gastric cancer (GC) are still unclear.</p><p><strong>Methods: </strong>GEO database, prognostic analysis, immune and single-cell analysis were used to explore the potential role of ENPP1 in GC. Electron microscopy, nanoparticle-tracking analysis identification and WB detection of marker proteins were used to verify the sEVs. Immunohistochemical staining, immunofluorescence staining, cell co-culture and flow cytometry were used to investigate the relationship among GC-derived sEVs-carried ENPP1 and dendritic cells (DCs) activation and TLS formation. Mice xenograft tumor model was used to explore the influence of sEVs-carried ENPP1 on vivo changes.</p><p><strong>Results: </strong>ENPP1 was highly expressed in GC tissues and cell lines and was associated with immune regulation. Immunohistochemistry showed that sEVs-carried ENPP1 expression was negatively correlated with the infiltration of DCs and CD8⁺T cells and the number of TLS in GC. Co-culture experiment showed that sEVs-carried ENPP1 could hydrolyze 2'3'-cGAMP and could be taken up by DCs. Inhibiting sEVs-carried ENPP1 expression promoted DCs' activation. Inhibition of sEVs-carried ENPP1 expression reduced the growth volume and weight of transplanted tumors in 615 mice, while increasing the activation of DCs, CD8⁺T cells, TLS and the formation of high endothelial venules.</p><p><strong>Conclusions: </strong>SEVs-carried ENPP1 regulates DCs' activation to inhibit TLS formation in GC. Our study illumes a new interaction mechanism between tumor cells and the immune microenvironment in GC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1419-1430"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148225936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"Escherichia coli as a gut microbial marker of obesity and its reduction following bariatric treatment\": ecological and functional perspectives.","authors":"Yimeng Zhou, Xue Meng","doi":"10.1007/s00535-026-02410-8","DOIUrl":"10.1007/s00535-026-02410-8","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1512-1513"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to \"Comment on \"Escherichia coli as a gut microbial marker of obesity and its reduction following bariatric treatment\": ecological and functional perspectives\".","authors":"Tomoyuki Hayashi, Noriho Iida","doi":"10.1007/s00535-026-02511-4","DOIUrl":"10.1007/s00535-026-02511-4","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1514-1515"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}