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Life sciences · Journal article
Gut Microbes · October 19, 2026
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Acute liver injury (ALI) is a severe clinical condition that can progress to chronic liver failure, cirrhosis, or hepatocellular carcinoma, yet therapeutic options remain limited. Here, we investigated how hepatotoxin-induced gut-liver dysbiosis drives hepatic inflammation through microbial crosstalk. Using three murine ALI models, we assessed liver injury, intestinal barrier integrity, microbial composition along the gut-liver axis, and immune activation. Each hepatotoxin recapitulated distinct features of human ALI and induced unique patterns of hepatic and intestinal injury, enabling the progressive translocation of live bacteria from the gut to the liver and bloodstream. ALI was consistently associated with depletion of commensal taxa (Lactobacillaceae, Ruminococcaceae, and Bifidobacteriaceae) and enrichment of opportunistic pathogens (Enterococcaceae, Clostridiaceae, Enterobacteriaceae, and Burkholderiaceae). Dysbiosis also involved reduced gut bacteriophages and the expansion of viral families, including Retroviridae and Herpesviridae, in the liver and blood. Transplantation of the fecal or liver microbiota from ALI mice into microbiota-depleted recipients reproduced liver injury, immune activation, and intestinal barrier disruption, demonstrating that dysbiotic microbial communities alone are sufficient to trigger hepatic inflammation. These communities activated Th1/Th17 associated pathways (NF-κB, IL-17, TGF-β, and antigen presentation networks) and expanded pro-inflammatory immune populations. A key advance of this study is the direct comparison of fecal- versus liver-derived microbiota, revealing distinct mechanistic roles for each in driving liver pathology. Across all models, hepatotoxin-induced intestinal barrier breakdown drives gut-liver dysbiosis, microbial translocation, and immune-mediated liver injury. These findings uncover a unifying mechanism by which microbial imbalance reprograms hepatic immunity and accelerates ALI progression.