Aflatoxin B1, Gut Microbiota Dysbiosis, and the Intestinal Barrier: Implications for the Gut–Liver Axis and Extrahepatic Cancer Risk

Aflatoxin B1 (AFB1) is a potent foodborne mycotoxin classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC) and is widely recognized for its causal role in hepatocellular carcinoma (HCC). Beyond its well-established hepatotoxicity, increasing evidence indicates that AFB1 also disrupts intestinal homeostasis by impairing epithelial barrier integrity, reducing mucus production, altering gut microbial composition, and disturbing microbial metabolism. These changes promote increased intestinal permeability, facilitating the translocation of bacteria and microbial products and contributing to chronic inflammation through the gut–liver axis. Recent experimental studies further suggest that alterations in short-chain fatty acid (SCFA) production and microbiota-dependent signaling pathways may actively mediate AFB1-induced intestinal and hepatic injury. Although direct evidence linking AFB1-induced dysbiosis to extrahepatic carcinogenesis remains limited, growing evidence indicates that persistent barrier dysfunction, microbial imbalance, and chronic inflammation may create a microenvironment favorable for tumor initiation and progression in tissues beyond the liver. This review critically summarizes current evidence regarding the effects of AFB1 on intestinal barrier function, gut microbiota dysbiosis, bacterial translocation, microbial metabolites, and the gut–liver axis while evaluating the mechanistic evidence supporting these interactions and highlighting the major knowledge gaps that should be addressed in future research.