Acute liver injury is triggered by dysbiosis and microbial translocation involving gut–liver axis

, 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.