Probiotic-derived extracellular vesicles protect against aflatoxin B1-induced inflammatory intestinal injury by remodelling the gut microbiota and activating intestinal AHR/IL-22 signalling in mice

Abstract

Abstract Background Aflatoxin B1 (AFB1) is a mycotoxin that widely exists in the environment and mouldy foods. The organ initially targeted by AFB1 is the intestine, and AFB1-induced intestinal injury cannot be ignored. Lactobacillus amylovorus, a predominant species of Lactobacillus, exerts carbohydrate metabolic functions. Extracellular vesicles (EVs), small lipid membrane vesicles, are widely involved in diverse cellular processes. However, the mechanism by which Lactobacillus amylovorus-QC1H-derived EVs (LA.EVs) protects against AFB1-induced intestinal injury remains unclear. Results In our study, a new strain named Lactobacillus amylovorus-QC1H (LA-QC1H)was isolated from pigfaeces. Then, EVs derived from LA-QC1H were prepared by ultracentrifugation. Our study showedthat LA.EVs significantly alleviated AFB1-induced inflammatory intestinal injury by inhibiting the production of proinflammatory cytokines and decreasing intestinal permeability. Meanwhile, 16S rRNA analysis showed that LA.EVs remodelled AFB1-induced gut dysbiosis in mice. However, LA.EVs failed to exert beneficial effects in antibiotic-treated mice. LA.EVs treatment resulted in higher intestinal levels of indole-3-acetic acid(IAA) and activating intestinal aryl hydrocarbon receptor (AHR)/IL-22 signalling in AFB-exposed mice. Inhibition of intestinal AHR signalling markedly weakenedthe protective effect of LA.EVs in AFB-exposed mice. Conclusions LA.EVs alleviated AFB1-induced inflammatory intestinal injury by remodelling the gut microbiota and activating intestinal AHR/IL-22 signalling in mice. Our study provides a new strategy for using LA.EVs as a therapeutic method to prevent AFB1-induced inflammatory intestinal injury.