Clostridium butyricumprotects the epithelial barrier by maintaining tight junction protein expression and regulating microflora in a murine model of dextran sodium sulfate-induced colitis

Objective: To investigate the protective effects of Clostridium butyricum on the epithelial barrier in dextran sodium sulfate (DSS)-induced colitis.Methods: Eight-week-old BALB/c mice were divided into a healthy control group and DSS-induced groups, including negative control (normal saline), 5-aminosalicylic acid (5-ASA), C. butyricum group, and 5-ASA + C. butyricum groups. Colitis was induced by 5% DSS ad libitum for 7 d. We assessed the disease activity index (DAI), histological grading, and ultrastructural changes by transmission electron microscopy. Stools were collected for bacterial microflora analysis. Tight junction (TJ) proteins, including claudin-1, claudin-2, occluding, and zonula occludens-1, were detected by immunohistochemical staining and western blot. We also assessed NF-κB and cytokines, including IL-1β, IL-13, and IL-10, by western blot.Results: C. butyricum decreased DAI and histological injury scores in DSS-induced mice, and repaired the damaged structure of TJs. Moreover, C. butyricum exerted its regulatory effect on fecal microflora by increasing and decreasing the growth of Lactobacillus spp. and Enterococcus spp., respectively, in the colon lumen. Expression levels of claudin-1, occludin and zonula occludens-1 were also elevated by the administration of C. butyricum. In addition, C. butyricum increased the expression of the anti-inflammatory cytokine, IL-10, and decreased levels of pro-inflammatory cytokines, including IL-1β, TNF, and IL-13, as well as NF-κB. Moreover, the beneficial effects of C. butyricum combined with 5-ASA were superior to treatment with C. butyricum only.Conclusion: In a mouse model of ulcerative colitis (UC), C. butyricum exerted a protective effect on the epithelial barrier by regulating microflora, maintaining the expression of TJ proteins and exerting immunoregulatory effects.