Fumonisins B1 exposure triggers intestinal tract injury via activating nuclear xenobiotic receptors and attracting inflammation response

Fumonisins (FBs) are mycotoxins that are widely distributed in crops and feed, and ingestion of FBs -contaminated crops is harmful to animal health. Furthermore, it is unknown if Fumonisins B1 (FB1) can cause intestinal toxicity. To investigate FB1-induced intestinal toxicity, mice were treated with 0 or 5 mg/kg FB1 by gavage administration for 42 days. Histopathology indicated that FB1 exposure caused proliferation of intestinal epithelial cells, intestinal villi and epithelial layer shedding, intestinal gland atrophy, and necrosis. Notably, FB1 interfered with nuclear xenobiotic receptors (NXR) homeostasis by regulating the level of aryl hydrocarbon receptor (AHR), constitutive androstane receptor (CAR), pregnane X receptor (PXR) and downstream target genes (CYP450s). Moreover, abnormal expression of inflammatory cytokines (IL-1β, IL-2, IL-4, IL-10, and TNF-α) indicated the occurrence of inflammation. The present study provides new insights regarding the mechanism of FB1-induced intestinal toxicity through activating the NXR system and by triggering inflammatory responses in the intestinal tract in mice. [Display omitted] •Fumonisin B1 induces AHR, CAR, PXR protein levels increase in cecum and colon of mice.•Fumonisin B1 exposure increases numbers of neutrophils and lymphocytes in duodenum, ileum, cecum and colon of mice.•IL-1β, IL-2, IL-4, IL-10 and TNF-α cytokines levels are significantly disturbed in intestinal tract exposed to fumonisin B1.