Inhibition, Gastritis Attenuation, and Gut Microbiota Protection in C57BL/6 Mice by NCUH062003.

(), one of the most prevalent pathogenic bacteria worldwide, is the leading cause of gastritis, gastric intestinal metaplasia, and gastric cancer. Antibiotics, the conventional treatment for eliminating , often lead to severe bacterial resistance, gut dysbiosis, and hepatic insufficiency and fail to address the inflammatory response or gastric mucosal damage caused by infection. In this study, based on 10-week animal experiments, two models of NCUH062003 for the prophylaxis and therapy of infection in C57BL/6 mice were established; a comprehensive comparative analysis was performed to investigate the anti- effect of probiotics, the reduction in inflammation, and repair of gastric mucosal damage. ELISA, immunohistochemistry, and pathology analyses showed that NCUH062003 decreased the expression of pro-inflammatory cytokine interleukins (IL-1β, IL-6) and myeloperoxidase (MPO) and reduced neutrophil infiltration in the gastric mucosa lamina propria. Immunofluorescence and biochemical analysis showed that NCUH062003 resisted gastric epithelial cell apoptosis, increased the level of superoxide dismutase (SOD) in gastric mucosa, and promoted the expression of tight junction protein ZO1 and Occludin. In addition, through high-throughput sequencing, in the probiotic therapy and prophylactic mode, the diversity and composition of the gut microbiota of HP-infected mice were clarified, the potential functions of the gut microbiota were analyzed, the levels of short-chain fatty acids (SCFAs) were measured, and the effects of NCUH062003 on the gut microbiota and its metabolites in HP-infected mice treated with amoxicillin/metronidazole were revealed. This study provides functional strain resources for the development and application of microbial agents seeking to antagonize beyond antibiotics.