Mucosal Defense and Repair

Several defense and repair mechanisms are responsible for preventing mucosal damage and subsequent ulcer formation. Mucus gel, through its buffering action, is the primary source of defense for the gastric epithelial surface against gastric acid. It allows an acidic environment to be maintained in the lumen but a near neutral pH to be maintained on the epithelial lining. On the epithelial lining, a number of protect ive mechanisms are responsible for the repair ofdamaged cells, production ofdefense mechanisms, and the promotion of epithelial growth.

PGs inhibit gastric acid secretion and have numerous mucosal protective effects, the most important of which include the stimulation of both mucus and phospholipid production, promotion of bicarbonate secretion, and increased mucosal cell turnover. Damage to the mucosal defense system is the primary method by which H. pylori or NSAIDs cause peptic ulcers.

Helicobacter pylori

H. pylori are a gram-negative microaerophilic rod that has a number of adaptive functions allowing it to live within the acidic environment of the stomach. It is an S-shaped bacterium with multiple flagella that initially inhabits the gastric antrum but migrates to the more proximal sections of the stomach over time. The motility provided by the flagella allows it to penetrate the mucous gel barrier, thus permitting a direct interaction with epithelial cells—the site where acute infection occurs. H. pylori are able to survive in the acidic conditions of the stomach because of its ability to induce a transient hypochlorhydria via production of urease, an enzyme that hydrolyzes urea into carbon dioxide and ammonia. Ammonia can both protect H. pylori and damage tissue.

A number of host and pathogenic factors contribute to the ability of H. pylori to cause gastroduodenal mucosal injury including: (a) direct mucosal damage; (b) alterations to host inflammatory responses; and (c) hypergastrinemia leading to a state of elevated acid secretion. Bacterial-surface adhesion components facilitate binding of H. pylori to epithelial cells, and vacuolating cytotoxin (vac A) facilitates the binding ofH. pylori to the cell membrane, thus enabling the H. pylori organism better access to nutrients. The cag pathogenicity island (cag-PAI) leads to the release of cytokines thus leading to a chronic inflammatory state in H. pylori-infected patients. The complex interplay between bacterial virulence factors and an enhanced inflammatory response results in a chronic H. pylori infection that elevates acid production and reduces various protective factors.

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