While Helicobacter pylori is a fundamental risk factor, gastric cancer (GC) aetiology involves combined effects of microbial (both H. pylori and non-H. pylori), host and environmental factors. Significant differences exist between the gastric microbiome of those with gastritis, intestinal metaplasia and GC, suggesting that dysbiosis in the stomach is dynamic and correlates with progression to GC. Most notably, a consistent increase in abundance of lactic acid bacteria (LAB) has been observed in GC patients including Streptococcus, Lactobacillus, Bifidobacterium and Lactococcus. This review summarises how LAB can influence GC by a number of mechanisms that include supply of exogenous lactate —a fuel source for cancer cells that promotes inflammation, angiogenesis, metastasis, epithelial-mesenchymal transition and immune evasion—, production of reactive oxygen species and N-nitroso compounds, as well as anti-H. pylori properties that enable colonization by other non-H. pylori carcinogenic pathobionts.

尽管幽门螺杆菌是基本的危险因素，但胃癌（GC）的病因涉及微生物（幽门螺杆菌和非幽门螺杆菌），宿主和环境因素的综合作用。胃炎，肠上皮化生和胃癌患者的胃微生物组之间存在显着差异，表明胃中的营养不良是动态的，并与胃癌的进展相关。最值得注意的是，在包括链球菌，乳杆菌，双歧杆菌和乳球菌在内的GC患者中观察到乳酸菌（LAB）的丰度持续增加。。这篇综述总结了LAB如何通过多种机制影响GC，包括提供外源性乳酸（一种促进炎症，血管生成，转移，上皮-间质转化和免疫逃逸的癌细胞燃料来源），活性氧和N的产生-亚硝基化合物，以及抗幽门螺杆菌的特性，使其能够被其他非幽门螺杆菌致癌性病原体定殖。