Deoxynivalenol Exposure Induced Colon Damage in Mice Independent of the Gut Microbiota

Scope: To investigate whether deoxynivalenol (DON) can induce intestinal damage through gut microbiota in mice. Methods and results: Mice are orally administered DON (1 mg kg(-1) bw day(-1)) for 4 weeks, and then recipient mice receive fecal microbiota transplantation (FMT) from DON-exposed mice after antibiotic treatment. Furthermore, the mice are orally treated with DON (1 mg kg(-1) bw day(-1)) for 4 weeks after antibiotic treatment. Histological damage, disruption of tight junction protein expression, and increased oxidative stress and apoptosis in the colon as well as higher serum lipopolysaccharides are observed after DON exposure. Moreover, DON exposure changes the composition and diversity of the gut microbiota as well as the contents of fecal metabolites (mainly bile acids). Differential metabolic pathways may be related to mitochondrial metabolism, apoptosis, and inflammation following DON exposure. However, only a decrease in mRNA levels of occludin and claudin-3 is observed in the colon of recipient mice after FMT. After depleting the gut microbiota in mice, DON exposure can also cause histological damage, disorders of tight junction protein expression, and increased oxidative stress and apoptosis in the colon. Conclusions: DON exposure can induce colon damage in mice independent of the gut microbiota.

Automated summary

This study investigates whether deoxynivalenol (DON) can induce intestinal damage through gut microbiota in mice. The results show that DON exposure causes colon tissue damage, disruption of tight junction protein expression, increased oxidative stress and apoptosis in mice. DON exposure also alters the composition and diversity of the gut microbiota as well as the contents of fecal metabolites. Only a decrease in specific gene expression levels in the colon is observed after fecal microbiota transplantation. Additionally, depleting the gut microbiota in mice also results in histological damage and disrupted tight junction protein expression in the colon after DON exposure.