[Studies on gastric mucosal cell injury induced by Helicobacter pylori].

The cause of gastric mucosal cell injury induced by Helicobacter pylori (H. pylori) was investigated in vitro using gastric mucosal cells derived from the stomach of male Japanese white rabbits. In order to evaluate the contribution of potent urease activity of H. pylori to gastric mucosal cell injury, supernatant of H. pylori bacterial pellet solubilized in a 1.0% solution of n-octyl-glucoside, the H. pylori extracts, was added to the rabbit gastric mucosal cell suspension. Cell injury was expressed by LDH release into the extracellular fluid of gastric mucosal cell suspension after 30 minutes incubation at 37 degrees C. Treatment of cells by H. pylori extracts (final concentration of 0.54 mg/ml) together with urea (final concentration at 50 mM) showed a high LDH release into the extracellular fluid suggesting definite gastric mucosal cell injury. Elevation of ammonia concentration and that of extracellular fluid pH were also observed by the treatment, whereas H. pylori extracts alone and urea solution alone did not. The ammonia concentration of extracellular fluid and LDH release were distinctly elevated in accord with increasing amount of H. pylori extracts under the existence of 50 mM urea. The degree of LDH release from gastric mucosal cell by H. pylori extracts under the existence of urea was similar to that induced by the administration of the same amount of exogenous ammonia. The addition of acetohydroxamic acid (AHA), a potent specific urease inhibitor, remarkably inhibited dose dependently the ammonia production, the elevation of pH of extracellular fluid and LDH release induced by H. pylori extracts under the presence of urea. These results suggest that the ammonia produced by potent urease activity of H. pylori under the presence of urea played an important role in the pathogenesis of gastric mucosal cell injury.