Although the use of the probiotic bacterium Lactobacillus for the treatment and prevention of diseases caused by various pathogenic bacteria has received increasing attention in recent years, its mechanism remains incompletely understood. Levilactobacillus brevis 23017 is a select probiotic strain that can regulate the immunity of host animals and resist pathogen
infections. In this study, we analyzed the effect of L. brevis 23017 on Yersinia enterocolitica intestinal
infection in a BALB/c mouse model and discussed its underlying mechanism. We found that in the mouse model, L. brevis 23017 prevented the damage of villi in the small intestine and decelerated
weight loss after Y. enterocolitica
infection. Moreover, we focused on the mechanism of the protective effect of L. brevis 23017 from the perspective of the damage and repair of the intestinal mucosal barrier. We observed that L. brevis 23017 maintained a normal mucosal barrier by altering the expression of
tight junction proteins. Notably, our results indicated that L. brevis 23017 effectively promoted the secretion of the intestine-specific
secretory immunoglobulin A (
SIgA) by B cells via regulating
cytokines and oxidative damage levels. This mechanism may be the reason for its protective role in Y. enterocolitica
infection. In addition, our results demonstrated that the mechanism of L. brevis 23017 was related to antibacterial colonization and
inflammation regulation and closely related to antioxidative stress and
SIgA promotion. The protective effect of L. brevis 23017 on mice was related to the signaling pathway
protein p38 MAPK and the phosphorylation levels of NF-κB. Our study provided novel insight into the mechanism of Lactobacillus against pathogenic
bacterial infections. Such insight is of great importance for the prevention, diagnosis, and treatment of related diseases.