HELICOBACTER-PYLORI AND GASTRIC-ACID - BIOLOGICAL AND THERAPEUTIC IMPLICATIONS

Helicobacter pylori is highly adapted to its unusual ecological niche in the human stomach. Urease activity permits H. pylori survival at a pH of <4 in vitro and is required for the organism to colonize in anim al models. However, urease does not play an important role in the surv ival of the organism in a pH range between 4 and 7. Other mechanisms o f pH homeostasis remain poorly understood, but preliminary studies ind icate that novel proteins are produced when H. pylori cells are shifte d from pH 7 to 3, and the gene encoding a P-type adenosine triphosphat ase that may catalyze NH4+/H+ exchange across the cytoplasmic membrane has been cloned. Mechanisms of pH homeostasis in other enteric bacter ia are reviewed and provide insight into additional pathways that may be used by H. pylori. An important adaptation of H. pylori to the gast ric environment may be its ability to alter gastric acid secretion. Ac ute infection is associated with transient hypochlorhydria, whereas ch ronic infection is associated with hypergastrinemia and decreased soma tostatin levels. Thus, the survival of H. pylori in the gastric enviro nment may be attributed to both the development of specialized intrins ic defenses and the organism's ability to induce physiological alterat ions in the host environment.