Valenzuela Manuel, Cáceres Aníbal, Almarza Oscar, Bravo Denisse, Soto Sarita, Cerda Oscar, Toledo Héctor
Faculty of Medicine, Department of Molecular and Cellular Biology, Laboratory of Molecular Microbiology, ICBM, University of Chile, Santiago, Chile; Toxicology and Cancer Biology Research Group, Louvain Drug Research Institute, Université Catholique de Louvain, Bruxelles, Belgium.
Helicobacter. 2014 Jun;19(3):182-93. doi: 10.1111/hel.12115. Epub 2014 Mar 17.
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.
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.
Indeed, speA mRNA and protein expression are acutely induced by acid stress.
Moreover, we showed that H. pylori uses arginine in an acid response mechanism required for its growth in acid conditions.
Altogether, these results provide novel information regarding the H. pylori physiology and acid response mechanism.
