{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T22:18:13Z","timestamp":1783117093280,"version":"3.54.6"},"reference-count":56,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"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":["Anim Models and Exp Med"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Gut barrier integrity prevents microbial translocation and systemic infection. Chronic alcohol disrupts this barrier, but its role in infection susceptibility among immune\u2010compromised hosts remains unclear. We investigated how chronic alcohol promotes gut barrier dysfunction, endotoxemia, and dysbiosis, predisposing to bacterial translocation and sepsis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Twenty\u2010four\u2010week\u2010old female Fc\u03b3RIIb\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      and wild\u2010type mice received oral gavage of 35% ethanol (4.2\u2009g\/kg\/day) or water for 10\u2009weeks. Gut barrier integrity was assessed by serum endotoxin, FITC\u2010dextran permeability, ileal claudin\u20101, and intestinal IgG\/neutrophil infiltration. Systemic inflammation was evaluated by serum TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106; gut microbiota by 16S rRNA sequencing. Bone marrow\u2013derived macrophages and hepatocytes from both genotypes were stimulated with LPS or ethanol to assess inflammatory responses, mitochondrial damage, and cGAS\u2010STING activation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Chronic alcohol induced gut barrier dysfunction in both groups, with more severe effects in Fc\u03b3RIIb\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice, which showed marked increases in serum endotoxin and FITC\u2010dextran permeability, reduced claudin\u20101, and enhanced intestinal IgG deposition with neutrophil accumulation. Serum TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106 were significantly elevated, reflecting a sepsis\u2010like profile. Alcohol induced dysbiosis with an increased Firmicutes\u2010to\u2010Bacteroidota ratio, elevated Lachnospiraceae, and reduced\n                      <jats:italic>Alistipes<\/jats:italic>\n                      ,\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      , and\n                      <jats:italic>Odoribacter<\/jats:italic>\n                      . In\u00a0vitro, LPS elicited stronger inflammation than ethanol in both cell types, with Fc\u03b3RIIb\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      cells producing greater cytokine levels. Both stimuli caused comparable mitochondrial damage and cGAS\u2010STING activation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Alcohol\u2010induced gut barrier dysfunction, endotoxemia, and dysbiosis predispose to bacterial translocation and early sepsis, particularly in hosts with impaired inhibitory Fc\u03b3 receptor signaling, supporting gut barrier preservation as a strategy for preventing alcohol\u2010associated infections and sepsis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ame2.70218","type":"journal-article","created":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T06:40:55Z","timestamp":1778308855000},"page":"967-979","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Chronic alcohol consumption compromises gut barrier integrity and promotes endotoxemia: Implications for sepsis susceptibility in immunocompromised hosts"],"prefix":"10.1002","volume":"9","author":[{"given":"Thansita","family":"Bhunyakarnjanarat","sequence":"first","affiliation":[{"name":"Department of Microbiology, Faculty of Medicine Chulalongkorn University  Bangkok Thailand"},{"name":"Faculty of Medicine, Center of Excellence on Translational Research in Inflammation and Immunology (CETRII) Chulalongkorn University  Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chatsuree","family":"Suksamai","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Faculty of Medicine Chulalongkorn University  Bangkok Thailand"},{"name":"Faculty of Medicine, Center of Excellence on Translational Research in Inflammation and Immunology (CETRII) Chulalongkorn University  Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dhammika 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