Corneal transcriptomic signatures of mycotoxin exposure reveal distinct immune and metabolic responses.

Fungal keratitis (FK) is a vision-threatening infection in which Fusarium species not only invade the cornea but may also release mycotoxins that exacerbate tissue injury. Here, we established a corneal exposure model to delineate the direct effects of Fusarium-derived mycotoxins independent of live fungal infection, using deoxynivalenol (DON), fumonisin B1 (FB1), and T-2 toxin as representative compounds. Hstological analyses revealed that all three mycotoxins markedly impaired corneal epithelial repair, induced stromal disorganization, and promoted inflammatory cell infiltration. At the molecular level, toxin exposure consistently activated immune-related pathways, including cytokine-cytokine receptor interaction, chemokine signaling, and IL-17 signaling, while concurrently suppressing metabolic and detoxification pathways such as cytochrome P450-mediated drug and xenobiotic metabolism. Despite these shared pathogenic features, each mycotoxin exhibited specific regulatory signatures, with T-2 toxin inducing the most pronounced transcriptomic disruption. These findings demonstrate that Fusarium mycotoxins are sufficient to drive corneal inflammation and tissue damage, providing mechanistic insight into mycotoxin-associated corneal injury.