Gastric secretion urease

This Gram-negative, microaerophilic bacterium infects areas of the stomach and duodenum it can result in peptic ulcers, gastritis, duodenitis and cancers. H. pylori s hehcal shape and flagella favour its motility in the mucus layer. Adhesins are produced by the bacterium, which binds to membrane-associated lipids and carbohydrates to maintain its attachment to epithelial cells. Large amounts of the enzyme urease are produced, both inside and outside of the bacterium. Urease metabolises urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (which neutralises gastric acid), and is instrumental in the survival of the bacterium in the acidic environment. 

In recent years, infection of the stomach with Helicobacter pylori which disrupts the normal inhibitory control for acid secretion resulting in excess acid destroying the mucosal barrier has been understood to be the main cause of gastric ulcers [147]. Excessive acid secretion in the stomach and reduction in gastric mucosal blood flow are considered responsible for ulcer formatimi. The colonization of H. pylori in the stomach is associated with a phospholipase likely to damage the protective layer of stomach. H. pylori thrives in the stomach by producing the enzyme urease. 

PPI treatment leads to dose-dependent inhibition of H. pylori in the stomach [11, 12]. The explanation for this effect comes from in vitro observations. At high pH values, in the presence of urea and a weak buffer, urease activity produces very high periplasmatic pH values which are bactericidal [13-16]. The detailed explanation of this mechanism is given in the chapter dealing with interactions between PPIs and H. pylori in vitro. This inhibition is, in our view, the major explanation of the adjuvant effect of PPIs during anti-i/. pylori therapy. Other effects, such as a PPI-induced increase of antibiotic secretion by the gastric epithelium [17] and a diminished inactivation of antibiotics by lowered gastric acid [18], may play a less important role. The suppressive effect of PPIs on H. pylori is the basis for anti-Helicobacter therapies with a PPI plus one or, preferably, two antibiotics [19, 20]. 

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