The interaction of pH, bile, and Helicobacter pylori may explain duodenal ulcer

Inhibition of Helicobacter pylori growth by bile suggests that it should be difficult for H. pylori to colonize the duodenum and cause duodenal ulcer. To search for a common mechanism, we investigated the relationship between H. pylori strain (duodenal ulcer vs gastritis), type of bile acid conjugate, and inhibition of H. pylori growth.

H. pylori isolates from patients with duodenal ulcer and from volunteers with asymptomatic gastritis (six each) were grown in brain heart infusion broth medium containing mixtures of glycocholate, taurocholate, glycodeoxycholate, taurodeoxycholate, glycochenodeoxycholate, and taurochenodeoxycholate with and without lecithin.

Synthetic human bile with or without lecithin inhibited H. pylori growth in a dose-dependent manner. There was no difference in inhibition between H. pylori gastritis and duodenal ulcer isolates. Glycine and mixed glycine and taurine-conjugated bile acids inhibited H. pylori more than taurine-conjugated bile acids (e.g., 51%, 67%, and 80% compared to 21%, 39%, and 46% for 1, 2, and 4 mM mixed conjugates compared with taurine conjugates, p < 0.05, respectively.

The ability of H. pylori to grow in the presence of taurine-conjugated bile acids and the precipitation of glycine but not taurine bile acid conjugates by acid may provide one missing link among inhibition of H. pylori by bile, acid secretion, ability of antisecretory therapy to accelerate ulcer healing, and the ability of H. pylori to colonize the duodenal bulb of ulcer patients, leading to duodenal ulcer. These data also explain the disparate results of previous investigations of the effect of bile reflux in the stomach on the presence of H. pylori.