Talebi Ghazaleh, Nabavi-Rad Ali, Sadeghloo Zahra, Doulberis Michael, Zali Mohammad Reza, Yadegar Abbas
Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroklinik, Private Gastroenterological Practice, Horgen, Switzerland.
Folia Microbiol (Praha). 2025 Apr 17. doi: 10.1007/s12223-025-01263-7.
The increasing rate of Helicobacter pylori (H. pylori) antibiotic resistance has attenuated the effectiveness of conventional antibiotic-based treatment regimens. This study was aimed at investigating the in vitro inhibitory effects of Lactobacillus reuteri (L. reuteri) strain I300 against H. pylori. The inhibitory effects of live L. reuteri I300 and its different formulations I300L, I300G, and I300T were examined on H. pylori adhesion and invasion to AGS cells. Auto-aggregation and co-aggregation assays and also scanning electron microscopy were performed, evaluating L. reuteri capacity to auto-aggregate and co-aggregate with H. pylori. RT-qPCR and ELISA were used to investigate the expression, and production level of inflammation-related cytokines TNF-α, IL-8, and IL-10. E-cadherin expression level was also measured, determining L. reuteri potential effect on AGS cells integrity. L. reuteri presented a time-dependent capacity to auto-aggregate and co-aggregate with H. pylori. Live L. reuteri and its formulations significantly reduced H. pylori adhesion and invasion of AGS cells. H. pylori treatment with L. reuteri reduced proinflammatory cytokines TNF-α and IL-8 production while increasing anti-inflammatory cytokine IL-10 production. L. reuteri promoted the epithelial cell-cell contact by upregulating E-cadherin expression. This study indicated L. reuteri I300 as a potential probiotic strain with co-aggregation capacity and inhibitory effects against H. pylori adhesion, invasion, and inflammation.
幽门螺杆菌（H. pylori）抗生素耐药率的不断上升削弱了传统抗生素治疗方案的有效性。本研究旨在调查罗伊氏乳杆菌（L. reuteri）I300菌株对幽门螺杆菌的体外抑制作用。研究了活的罗伊氏乳杆菌I300及其不同制剂I300L、I300G和I300T对幽门螺杆菌黏附及侵袭AGS细胞的抑制作用。进行了自聚集和共聚集试验以及扫描电子显微镜检查，评估罗伊氏乳杆菌与幽门螺杆菌自聚集和共聚集的能力。采用RT-qPCR和ELISA法研究炎症相关细胞因子TNF-α、IL-8和IL-10的表达及产生水平。还检测了E-钙黏蛋白的表达水平，以确定罗伊氏乳杆菌对AGS细胞完整性的潜在影响。罗伊氏乳杆菌呈现出与幽门螺杆菌自聚集和共聚集的时间依赖性能力。活的罗伊氏乳杆菌及其制剂显著降低了幽门螺杆菌对AGS细胞的黏附和侵袭。用罗伊氏乳杆菌治疗幽门螺杆菌可降低促炎细胞因子TNF-α和IL-8的产生，同时增加抗炎细胞因子IL-10的产生。罗伊氏乳杆菌通过上调E-钙黏蛋白的表达促进上皮细胞间的接触。本研究表明，罗伊氏乳杆菌I300是一种具有共聚集能力且对幽门螺杆菌黏附、侵袭和炎症具有抑制作用的潜在益生菌菌株。
