Exploration of gastric carcinogenesis from the relationship between bile acids and intestinal metaplasia and intragastric microorganisms (H. pylori and non-H. pylori).

Gastric cancer (GC) is a prevalent form of cancer, with Helicobacter pylori (H. pylori) infection being the most common risk factor. Recent studies have highlighted the role of long-term irritation of the gastric mucosa caused by bile reflux in the development of cancer. Bile acids (BAs), which are a significant component in bile reflux, have the potential to promote gastric carcinogenesis through various mechanisms. These mechanisms include the induction of intestinal metaplasia (IM), inhibition of H. pylori activity, modification of H. pylori colonization, and alteration of the abundance and composition of microorganisms in the stomach. Defining the mechanism of bile acid-induced gastric carcinogenesis could potentially be an effective approach to prevent GC. Hence, this paper aims to review the mechanism of bile acid-induced IM, the association between BAs and H. pylori infection as well as microorganisms in the stomach, and the correlation between BAs and gastric carcinogenesis. The ultimate goal is to elucidate the role of BAs in the development of GC.