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.
['Valenzuela|Manuel|M|', 'Cáceres|Aníbal|A|', 'Almarza|Oscar|O|', 'Bravo|Denisse|D|', 'Soto|Sarita|S|', 'Cerda|Oscar|O|', 'Toledo|Héctor|H|']
D000143:Acids D002262:Carboxy-Lyases D004361:Drug Tolerance D020869:Gene Expression Profiling D016480:Helicobacter pylori D006706:Homeostasis D006801:Humans D006863:Hydrogen-Ion Concentration
arginine decarboxylase speA Helicobacter pylori acidic pH adiA agmatine