As a common fungicide,
tebuconazole are ubiquitous in the natural environment and poses many potential risks. In this study, we examined the effects of exposure to
tebuconazole on
colitis in mice and explored its underlying mechanism. Specifically, exposure to
tebuconazole could cause structural damage and inflammatory cell infiltration in colon tissue, activate the expression of
inflammation-related genes, disrupt the expression of barrier function-related genes, and induce the colonic
inflammation in mice. Similarly, exposure to
tebuconazole could also exacerbate DSS-induced
colitis in mice. In addition, we found that
tebuconazole also could change the composition of the gut microbiota. In particular,
tebuconazole significantly increases the relative abundance of Akkermansia of mice. Moreover,
tebuconazole resulted in metabolic profiles disorders of the serum, leading to significant changes in the relative contents of metabolites involving
glycolipid metabolism and
amino acid metabolism. Particularly, the results of the gut microbiota
transplantation experiment showed that exposure to
tebuconazole could induced colonic
inflammation in mice in a gut microbiota-dependent manner. Taken together, these results indicated that
tebuconazole could induce
colitis in mice via regulating gut microbiota. Our findings strongly support the concept that the gut microbiota is a key trigger of
inflammatory bowel disease caused by
pesticide intake.