The regulatory effect of Bifidobacterium dentium N8 on lipopolysaccharide-induced intestinal mucosal immune injury.

This study aimed to evaluate the regulatory effect of Bifidobacterium dentium N8 on lipopolysaccharide (LPS)-induced intestinal mucosal immune injury in BALB/c mice. An acute LPS-induced inflammation model was established to observe changes in the intestinal morphology, barrier function, and immune status in mice following intervention with different doses of B. dentium N8. The results showed that LPS treatment significantly aggravated diarrhea in mice, increased the Disease Activity Index (DAI) score, damaged intestinal structure, reduced the number of goblet cells, and decreased the expression of tight junction proteins. This was accompanied by increased serum levels of D-lactic acid and diamine oxidase (DAO), decreased secretory IgA (sIgA) secretion, and dysregulated expression of inflammatory cytokines. Intervention with B. dentium N8 significantly ameliorated these injuries, manifested as a marked reduction in diarrhea symptoms and disease activity index scores, alleviated histopathological damage, repaired barrier function (evidenced by decreased serum D-lactate and DAO levels), enhanced sIgA expression, and a rebalanced profile of inflammatory cytokines. Moreover, the high-dose intervention group showed better effects than the low-dose group. The study indicates that B. dentium N8 plays a positive role in alleviating LPS-induced intestinal mucosal immune injury by enhancing barrier function, promoting mucosal immunity, and regulating inflammatory responses, suggesting its potential application value in improving intestinal inflammatory diseases.