{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T13:50:53Z","timestamp":1790344253930,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T00:00:00Z","timestamp":1774828800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T00:00:00Z","timestamp":1774828800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2026,5]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background<\/jats:title>\n Gut microbiota, microbial metabolites, and inflammatory cytokines play key roles in the pathogenesis of cirrhosis and hepatocellular carcinoma (HCC); however, data from Southeast Asia are limited. This study examined microbial composition, intestinal permeability, butyrate\u2010related gene expression, and cytokine profiles in Thai patients with cirrhosis, with and without HCC.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n This cross\u2010sectional study included 30 healthy controls, 33 patients with cirrhosis without HCC, and 44 patients with HCC (HCC\u2013cirr). Fecal samples were analyzed using 16S rRNA sequencing. Microbial functional profiles were predicted using KEGG Orthology\u2013based pathway inference. Gut permeability markers (intestinal fatty acid\u2013binding protein [I\u2010FABP] and lipopolysaccharide\u2010binding protein [LBP]), butyrate\u2010associated gene (BCoAT) expression, and cytokine profiles were assessed.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Alpha diversity (Chao1) was significantly lower in HCC\u2013cirr patients than in healthy controls (\n p<\/jats:italic>\n \u2009<\u20090.001) and patients with cirrhosis (\n p<\/jats:italic>\n \u2009=\u20090.008). Beta diversity also differed significantly between HCC\u2013cirr and controls (\n p<\/jats:italic>\n \u2009=\u20090.008).\n Ligilactobacillus<\/jats:italic>\n ,\n Catenibacterium<\/jats:italic>\n , and\n Alloprevotella<\/jats:italic>\n were enriched in the cirrhosis group, whereas HCC\u2013cirr patients showed increased\n \n Ruminococcus gnavus<\/jats:italic>\n <\/jats:styled-content>\n and reduced butyrate producers (\n Coprococcus<\/jats:italic>\n ,\n Subdoligranulum<\/jats:italic>\n ). Functional prediction suggested pathway differences between cirrhosis and HCC\u2013cirr, including folate, sulfur, tyrosine metabolism, and steroid biosynthesis. BCoAT expression was significantly decreased in HCC (\n p<\/jats:italic>\n \u2009=\u20090.006). Plasma LBP and I\u2010FABP were significantly elevated in HCC\u2013cirr (\n p<\/jats:italic>\n \u2009=\u20090.033,\n p<\/jats:italic>\n \u2009<\u20090.001), with I\u2010FABP also higher than in cirrhosis (\n p<\/jats:italic>\n \u2009=\u20090.002). Proinflammatory cytokines (GM\u2010CSF, IL\u201010, IL\u201018, IL\u20101\u03b1, IL\u20107, IL\u20108, and M\u2010CSF) were elevated in HCC\u2013cirr.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Among the Thai cohort, HCC with cirrhosis was associated with distinct gut microbial changes, reduced BCoAT expression, increased gut permeability, and cytokine alterations, highlighting the contribution of gut dysbiosis and microbial by\u2010products to liver disease progression.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jgh.70358","type":"journal-article","created":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T11:10:16Z","timestamp":1774869016000},"page":"1590-1599","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Gut Microbiome Signatures Differ in Cirrhosis With and Without Hepatocellular Carcinoma in a Southeast Asian Cohort"],"prefix":"10.1111","volume":"41","author":[{"given":"Thananya","family":"Jinato","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Faculty of Medicine Chulalongkorn University Bangkok Thailand"},{"name":"Center of Excellence in Kidney\u2010Liver\u2010Microbiota, Faculty of Medicine Chulalongkorn University Bangkok Thailand"},{"name":"Mahidol Vivax Research Unit, Faculty of Tropical Medicine Mahidol University Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masoumeh","family":"Sikaroodia","sequence":"additional","affiliation":[{"name":"Microbiome Analysis Center George Mason University Manassas Virginia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick\u00a0M.","family":"Gilleveta","sequence":"additional","affiliation":[{"name":"Microbiome Analysis Center George Mason University Manassas Virginia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thasinas","family":"Dissayabutra","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Faculty of Medicine Chulalongkorn University Bangkok Thailand"},{"name":"Center of Excellence in Kidney\u2010Liver\u2010Microbiota, Faculty of Medicine Chulalongkorn University Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pisit","family":"Tangkijvanich","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Faculty of Medicine Chulalongkorn University Bangkok Thailand"},{"name":"Center of Excellence in Hepatitis and Liver Cancer, Faculty of Medicine Chulalongkorn University Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4928-3681","authenticated-orcid":false,"given":"Jasmohan\u00a0S.","family":"Bajaj","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology 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