The generation of ammonium hydroxide also leads to direct histologic damage. Hydroxide ion is directly cytotoxic and the ammonium ion may interfere with normal hydrogen ion back-diffusion across gastric mucosa. 13 Lipases, proteases, vacuolating cytotoxin, and growth-inhibitory factors. A number of other substances elaborated by H. pylori contribute to its pathogenic effect on the gastric mucosa. Phospholipase A2 and lipase lead to loss of lysophospholipid generation, mucus lipid degradation, and disruption of mucus gel integrity.
Proteases disrupt the structure of mucin.
The combined effects of these proteases and lipases is increased susceptibility to damage from the low pH and pepsin present in the gastric lumen. GIF inhibits the proliferation of gastric epithelial cells. The exact mechanism is unknown but appears to be related to a component of bacterial protein that inhibits protein synthesis in the gastric cells. 14 Immune response. The presence of H. pylori in the stomach induces a chronic, active, inflammation in everyone infected.