Weizmannia coagulans BCF-01: a novel gastrogenic probiotic for Helicobacter pylori infection control

益生菌 生物 幽门螺杆菌 上睑下垂 失调 胃粘膜 微生物学 体内 胃炎 抗生素 TLR4型 炎症 肠道菌群 免疫学 细菌 炎症体 生物化学 遗传学 生物技术
作者
Zhenhui Chen,Ziyu Tang,Wendan Li,Xiaoshi Deng,Lijie Yu,Jixiang Yang,J.W. Liu,Yunshui Cheng,Wanwen Huang,Xiaoxiao Guo,Jidong Shan,Dian-Yuan Zhou,Weisen Zeng,Yang Bai,Hongying Fan
出处
期刊:Gut microbes [Informa]
卷期号:16 (1)
标识
DOI:10.1080/19490976.2024.2313770
摘要

The widespread prevalence of Helicobacter pylori infection, particularly in China, contributes to the development of gastrointestinal diseases. Antibiotics have limitations, including adverse reactions and increased antibiotic resistance. Therefore, identification of novel gastrogenic probiotics capable of surviving the acidic gastric environment and effectively combating H. pylori infection has potential in restoring gastric microbiota homeostasis. Five novel strains of human gastrogenic Weizmannia coagulans (BCF-01-05) were isolated from healthy gastric mucosa and characterized using 16S rDNA identification. Acid resistance, H. pylori inhibition, and adherence to gastric epithelial cells were evaluated in in-vitro experiments and the molecular mechanism explored in in-vivo experiments. Among the gastric-derived W. coagulans strains, BCF-01 exhibited the strongest adhesion and H. pylori inhibition, warranting further in-vivo safety evaluation. Through 16S rRNA sequencing of a mouse model, BCF-01 was determined to significantly restore H. pylori-associated gastric dysbiosis and increase the abundance of potential probiotic bacteria. Furthermore, BCF-01 enhanced mucosal tight junction protein expression and inhibited the TLR4-NFκB-pyroptosis signaling pathway in macrophages, as demonstrated by qRT-PCR and western blotting.These findings highlight the potential of BCF-01 in the prevention and control of H. pylori infection. Specifically, treatment with BCF-01 effectively restored gastric microecology and improved H. pylori-mediated mucosal barrier destruction while reducing inflammation through inhibition of the TLR4-NFκB-pyroptosis signaling pathway in macrophages. BCF-01 is a promising alternative to traditional triple therapy for H. pylori infections, offering minimal side effects with high suitability for high-risk individuals.
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