Figure 1.

The interplay between H. pylori and the gut microbiota. Infection with H. pylori causes and maintains an inflammatory response in the gastric mucosa, which leads to the loss of acid-secreting parietal cells and an elevation in gastric pH in certain infected people. H. pylori colonization declines in this changing environment and bacteria from other parts of the gut colonize the gastric niche, resulting in gut dysbiosis. Non-H. pylori bacteria promote gastric carcinogenesis through their own characteristics and microbial metabolites, such as N-nitroso compounds and lactate. The main putative mechanisms include induction of inflammatory response, modulation of the immune response, induction of DNA damage, and development of carcinogenesis.