Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Helicobacter. 2021 Jun;26(3):e12806. doi: 10.1111/hel.12806. Epub 2021 Apr 11.
Eradication of Helicobacter pylori infection is the most direct and effective way for preventing gastric cancer. Lactic acid bacteria are considered as alternative therapeutic agents against H. pylori infection.
Effects of Lactobacillus rhamnosus JB3 (LR-JB3) on the virulence gene expression of H. pylori and infection-induced cellular responses of AGS cells were investigated by co-cultivating infected AGS cells with different multiplicity of infections (MOIs) of LR-JB3.
LR-JB3, specifically at a MOI of 25, suppressed the association ability of H. pylori and its induced IL-8 levels, as well as the mRNA levels of vacA, sabA, and fucT of H. pylori, infection-induced Lewis (Le) antigen and Toll-like receptor 4 (TLR4) expressions in AGS cells. However, the apoptosis mediated by infection was inhibited by LR-JB3 in a dose-dependent manner. In addition, autoinducer (AI)-2 was observed to have increased the association ability and fucT expression of H. pylori, and Le antigen and TLR4 expression of AGS cells. Interestingly, an unknown bioactive cue was hypothesized to have been secreted from LR-JB3 at a MOI of 25 to act as an antagonist of AI-2.
LR-JB3 possesses various means to interfere with H. pylori pathogenesis and infection-induced cellular responses of AGS cells to fight against infection.
根除幽门螺杆菌感染是预防胃癌的最直接、最有效的方法。乳酸菌被认为是治疗幽门螺杆菌感染的替代治疗药物。
通过共培养感染 AGS 细胞与不同感染复数（MOI）的鼠李糖乳杆菌 JB3（LR-JB3），研究 LR-JB3 对幽门螺杆菌毒力基因表达和感染诱导的 AGS 细胞细胞反应的影响。
LR-JB3，特别是在 MOI 为 25 时，抑制了幽门螺杆菌的结合能力及其诱导的 IL-8 水平，以及幽门螺杆菌的 vacA、sabA 和 fucT 基因、感染诱导的 Lewis（Le）抗原和 Toll 样受体 4（TLR4）表达。然而，LR-JB3 以剂量依赖的方式抑制了由感染介导的细胞凋亡。此外，发现自诱导物（AI）-2 增加了幽门螺杆菌的结合能力和 fucT 表达，以及 AGS 细胞的 Le 抗原和 TLR4 表达。有趣的是，假设 LR-JB3 在 MOI 为 25 时分泌了一种未知的生物活性信号分子，作为 AI-2 的拮抗剂。
LR-JB3 具有多种干扰幽门螺杆菌发病机制和感染诱导的 AGS 细胞细胞反应的方法，以抵抗感染。
