Mechanistic evidence and assumptions in mycotoxin-gut interaction

Abstract

Mycotoxins are increasingly recognised as ecological mediators that act through a bidirectional gut–microbiota axis. Microbial metabolism governs toxin fate by driving detoxification, bioactivation, sequestration and deconjugation, whereas mycotoxin exposure reshapes microbial communities, disrupts epithelial barrier function and amplifies immune signalling. Across aflatoxin B1, ochratoxin A, fumonisin B1, deoxynivalenol and T-2 toxin, the microbiome emerges as both a determinant and a target of toxicity, with strain-level functional diversity influencing susceptibility, detoxification capacity and host outcome. A further consequence of chronic exposure may be selection for pathobionts and antibiotic-resistant populations, raising the possibility that mycotoxins contribute to microbiome instability beyond direct toxic effects. Despite these advances, most evidence remains correlative or model-specific, and causal validation in vivo is still limited. Integrating microbiology, metabolomics, epithelial biology and ecological theory is essential to understand these interactions and to better guide microbiome-informed strategies for mycotoxin exposure mitigation.