Clostridium butyricum 11 alleviates ulcerative colitis in mice by improving intestinal microbiota and inhibiting NLRP3 inflammasome assembly mediated by JAK2/STAT3 pathway

The soil is rich in microorganisms, particularly bacteria. Our previous studies have found that soil-derived Clostridium butyricum 11 (CB11) had a good antibacterial effect on Clostridium perfringens, which is the main pathogenic microorganism causing necrotizing enteritis in chickens. It could be deduced that CB11 may have a potential therapeutic effect on ulcerative colitis (UC). Therefore, this study aimed to evaluate the effect of CB11 on dextran sodium sulfate (DSS)-induced UC in C57BL/6 mice and its mechanism. The results showed that CB11 could significantly alleviate the pathological injury of the colon in UC mice, up-regulate the expression of colonic tight junction protein (TJs) and MUC2, and decrease MPO activity (P < 0.05). Compared with the Model group, CB11 significantly increased the antioxidant capacity (T-SOD, CAT, and GSH-Px) of UC mice and the related genes expression of oxidative stress (Nrf2, HO-1, and NQO1), decreased the secretion level of inflammatory factors (IL-1β, IL-6, IL-17A, IL-18, and TNF-α), and the related genes expression of Keap1 and apoptosis (Bax, Caspase 3, Caspase 8 and Caspase 9, P < 0.05). Additionally, CB11 significantly reversed the intestinal microbiota imbalance caused by DSS, including Bacteroides, Culturomica, Allobaculum, Parasutterella, Helicobacter, Mucispirillum, Ligilactobacillus, Obesimuribacter, etc. Furthermore, CB11 inhibited the activation of the JAK2/STAT3 pathway and the assembly of NLRP3 inflammasome in the colon. Fecal microbial transplantation (FMT) results verified that the intestinal microbiota regulated by CB11 markedly improved UC symptoms. These results suggested that CB11 could be utilized as a candidate probiotic to treat UC and is worthy of further research and application.