Helicobacter pylori (H. pylori) is a Gram negative microaerophilic bacteria whose only known niche is the human gastric mucosa. The presence of H. pylori is associated with various pathologies ranging from peptic ulcer disease to gastric carcinoma. H. pylori virulence is dependent on its exceptional ability to resist to the stomach acidity by hydrolyzing urea into ammonia. Survival of H. pylori to acidity in the presence of urea relies on the activity of a membrane protein, UreI.
Aims: We decided to better characterize the role of UreI (i) in vitro in ammonia production through the action of urease, and (ii) in vivo in the colonization of the gastric mucosa.
Methods: Ammonia production by a wild type strain of H. pylori or by a UreI-deficient strain was measured as a function of extracellular pH. In addition, the kinetics of elimination of a UreI-deficient mutant in vivo were realized in the mouse model for colonization.
Results: UreI was associated with an increase of ammonia production in acidic conditions in vitro and was necessary for the initial steps of the mouse stomach colonization.
Conclusion: UreI thus behaves as a sensor of extracellular pH. This protein activates urease at acidic pH; thereby, it probably allows H. pylori to resist to acidity in vivo during the first steps of infection.