Characterization of the arginine decarboxylase gene (ORF HP0422, speA) involved in acid tolerance in Helicobacter pylori.

Background: Helicobacter pylori is a motile microaerophilic bacterium that colonizes the human stomach. H. pylori infection triggers gastric diseases, such as gastritis, peptic ulcer and gastric cancer. Stomach represents a barrier for microorganism colonization, particularly because of its high hydrochloric acid concentration. The main mechanism developed by H. pylori to maintain intracellular pH homeostasis in this environment is the urease activity. However, urease negative strains can be also isolated from clinical samples, suggesting that H. pylori presents other components involved in acid resistance.

Objective: Here, we present some evidence that the arginine decarboxylase gene (speA) in H. pylori could be involved in an acid adaptation mechanism similar to the one in Enterobacteriaceae, which is dependent on the presence of arginine.

Methods: Indeed, speA mRNA and protein expression are acutely induced by acid stress.

Results: Moreover, we showed that H. pylori uses arginine in an acid response mechanism required for its growth in acid conditions.

Conclusion: Altogether, these results provide novel information regarding the H. pylori physiology and acid response mechanism.