Helicobacter pylori-associated gastritis is characterized by an abundant inflammatory response and gastric epithelial cell injury. Adherence of H. pylori to gastric epithelial cells seems to be required for bacterial colonization of the gastric mucosa. Attachment of the bacterium to polarized gastric epithelial cells causes damage to microvilli and stimulates actin polymerization, which is associated with adherence pedestal formation. Studies suggest that H. pylori directly contributes to the injury of gastric epithelial cells by the elaboration of cytotoxic factors. The first toxin identified from H. pylori strains, known as vacuolating cytotoxin, induces vacuole formation in eukaryotic cells. Elaborated enzymes by H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid. This cell injury may lead to cell death, believed to result from induction of apoptosis. There are sufficient data to suggest that H. pylori, through direct pathogenic mechanisms, contributes significantly to the gastric mucosal injury associated with this infection, and may enhance the susceptibility of gastric epithelial cells to carcinogenic conversion.
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