Gut microbiota dysbiosis transmits deoxynivalenol toxicity and triggers liver inflammation

• DON disrupts intestinal structure, alters microbial composition, and activates liver inflammation via the TLR4/MyD88/NF-κB pathway. • Liver inflammation was replicated in germ-free mice colonized with microbiota from DON-exposed donors. • Alloprevotella and Pseudomonas are key microbial drivers of microbiome induced liver inflammation effect. • Dysbiosis can independently trigger liver inflammation, highlighting a microbiota-mediated pathogenic mechanism in mycotoxin toxicity. Deoxynivalenol (DON), a mycotoxin produced by Fusarium species, is known to compromise gut barrier integrity and induce systemic inflammation. This study demonstrates that intestinal microbiota play a central role in DON-induced liver inflammation. Through oral exposure and fecal microbiota transplantation (FMT) experiments in mice, we observed that DON disrupts intestinal structure, alters microbial composition, and activates liver inflammation via the TLR4/MyD88/NF-κB pathway. Notably, liver inflammation was replicated in pseudo-germ-free mice colonized with microbiota from DON-exposed donors, even in the absence of direct DON exposure. Microbial analysis identified Alloprevotella , a mucin-degrading genus associated with increased intestinal permeability, and Pseudomonas , a pathogenic genus enriched in the liver, as key candidate microbial drivers of this effect. These findings underscore that dysbiosis, especially involving specific bacterial genera, can independently trigger liver inflammation, highlighting a microbiota-mediated pathogenic mechanism in mycotoxin toxicity.