Li Junyi, Xu Xiaoyan, Yang Shiyu, Liu Kui, Wu Min, Xie Mingyong, Xiong Tao
State Key Laboratory of Food Science and Resources, Nanchang University, No. 235 Nanjing East Road, Nanchang 330047, China.
School of Food Science & Technology, Nanchang University, No. 235 Nanjing East Road, Nanchang 330047, China.
Microorganisms. 2024 Dec 7;12(12):2521. doi: 10.3390/microorganisms12122521.
(), 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.
（）是全球最普遍的致病细菌之一，是胃炎、胃肠化生和胃癌的主要病因。抗生素作为消除（该细菌）的传统治疗方法，常常导致严重的细菌耐药性、肠道菌群失调和肝功能不全，并且无法解决由（该细菌）感染引起的炎症反应或胃黏膜损伤。在本研究中，基于为期10周的动物实验，建立了两种用于预防和治疗C57BL/6小鼠（该细菌）感染的NCUH062003模型；进行了全面的比较分析，以研究益生菌的抗（该细菌）作用、炎症减轻情况以及胃黏膜损伤的修复。酶联免疫吸附测定（ELISA）、免疫组织化学和病理学分析表明，NCUH062003降低了促炎细胞因子白细胞介素（IL-1β、IL-6）和髓过氧化物酶（MPO）的表达，并减少了胃黏膜固有层中的中性粒细胞浸润。免疫荧光和生化分析表明，NCUH062003抵抗胃上皮细胞凋亡，提高胃黏膜中超氧化物歧化酶（SOD）水平，并促进紧密连接蛋白ZO1和闭合蛋白的表达。此外，通过高通量测序，在益生菌治疗和预防模式下，阐明了幽门螺杆菌（HP）感染小鼠肠道微生物群的多样性和组成，分析了肠道微生物群的潜在功能，测量了短链脂肪酸（SCFAs）水平，并揭示了NCUH062003对阿莫西林/甲硝唑治疗的HP感染小鼠肠道微生物群及其代谢产物的影响。本研究为开发和应用超越抗生素的抗（该细菌）微生物制剂提供了功能菌株资源。
