Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via:A. Antral alkalinization leading to inhibition of somatostatin release
Helicobacter pylori possess the enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach. H. pylori infection is associated with decreased levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. These effects are probably mediated by H. pylori-induced local alkalinization of the antrum (antral acidification is the most potent antagonist to antral gastrin secretion), and H. pylorimediated increases in other local mediators and cytokines. The result is hypergastrinemia and acid hypersecretion, presumably leading to the parietal cell hyperplasia seen in many patients with duodenal ulcer. Other mechanisms whereby H. pylori can induce gastroduodenal mucosal injury include the production of toxins (vacA and cagA), local elaboration of cytokines (particularly interleukin-8) by infected mucosa, recruitment of inflammatory cells and release of inflammatory mediators, recruitment and activation of local immune factors, and increased apoptosis.