Pathogenesis

H. pylori is a gram-negative spiral bacterium that has developed the unique ability to colonize the gastric mucosa, which is usually well protected against bacterial infections. The H. pylori genome has been sequenced and contains a number of virulent factors that permits it to colonize the gastric mucosa [11]. The flagella of H. pylori allow it to be mobile in the mucous layer of the gastric epithelium. It also possesses urease, which has the ability to hydrolyze urea into carbon dioxide, and hydrate ammonia, thereby protecting the bacterium from an acid environment with an ammonia envelop. This enzyme activity is regulated by the pH in the immediate environment of the bacterium via a unique pH-gated urea channel (UREI). H. pylori also has a number of outer membrane proteins such as the BabA, HopZ and AlpAB proteins, which can mediate adhesions to gastric epithelial cells. The BabA protein has been shown to bind to Lewis B blood group antigen [12]. A significant proportion of H. pylori strains also possess the cag (cytotoxin-associated gene) pathogenicity island (837 kDa), which is a foreign piece of DNA that was acquired during its evolution. It is thought to encode for a type 4 secretion apparatus, a "molecular syringe" that translocates the CAG

protein into epithelial cells [13, 14]. This protein is phosphorylated intracel-lularly; its function is unknown but is thought to modify cellular response and cytokine production in host cells. In certain populations, the presence of this pathogenic island is associated with more severe disease. Also, a significant proportion of H. pylori strain secret vacuolating cytotoxin like an exotoxin. This toxin was named because it causes vacuous formations in epithelial cells infected with H. pylori strain producing this toxin. This cytotoxin has the ability to insert itself into epithelial cell membranes, forming channels in which bicarbonate and other organic ions can be released. This vacuolate toxin also targets mitochondrial membranes and may induce apoptosis via release of cytochrome c in certain populations, particularly in Western countries. Certain vacuolating gene variants are associated with more severe disease; however, this association has not been found in the Far East. Currently, the pathogenic role of these toxins is still not clear. It is now established that vacuolate is not essential for colonization. The pathogenesis of H. pylori has been reviewed by Hatakeyama and Brzozowski and by Kusters et al. [15, 16].

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