Recent evidence suggests that Helicobacter pylori can act outside stomach by influencing the gut microbiome. We hypothesize that interactions between H. pylori and the gut microbiome, and the resulting changes in the gut chemicals (bile acids and bacterial signaling molecules involved in quorum sensing, e.g., autoinducer-2/AI-2), influence pathogen survival, antibiotic response, and disease progression. Our gut microbiome, bile acid, and AI-2 analyses showed that H. pylori patients had decreased alpha diversity (p = 0.05), increased AI-2 concentration (p = 0.019), decreased taurine-conjugated bile acids, and increased unconjugated bile acids. A co-occurring module of Prevotella, Holdemanella, and Subdoligranulum, was higher in patients (p = 0.04) and relative abundance of Allisonella was positively associated with levels of unconjugated bile acids, chenodeoxycholic acid, and cholic acid (p = 0.05 and 0.02, respectively). Our study is the first to characterize the gut microbiome-metabolome signature (bile acids and AI-2) in H. pylori patients. Abundance of certain bacteria that deconjugate bile acids along with increased AI-2 possibly gives selective advantage for H. pylori growth, further reducing microbial diversity. Taurine-conjugated bile acids inhibit H. pylori growth. We propose a model describing interplay of these factors in H. pylori disease progression, suggesting therapeutic targets worth exploring with rising antibiotic resistance.
Alikhan et al. (Wed,) studied this question.