The enzyme is found readily on the surface and in the cytoplasm of the bacterium. Urease helps digest urea to produce ammonia and bicarbonate. Ammonia generated around the bacterial cells neutralizes gastric acid. This process benefits the bacterium, but is toxic to gastric epithelial cells. Pathogenicity Ammonia production from urease activity is toxic to mammalian cells.
Epithelial cells undergo vacuolation because of urease activity.
In addition, urease and other products of H. pylori , including protease, catalase, and phospholipases A2 and C, cause weakening of the mucous bicarbonate layer of the GI tract and damage to surface epithelial cells. LPS seems to inhibit glycosylation of mucus leading to a significant change in the macromolecular structure of mucin from high molecular weight to low molecular weight form. LPS may interfere with protective function of mucus layer and make epithelial cells at the surface vulnerable to acid. LPS from some strains of H. pylori stimulates secretion of pepsinogen. Lastovica et al showed that H. pylori is the only bacterium that stimulates pepsinogen secretion.