The human gastric pathogen Helicobacter pylori is able to establish an infection in a hostile environment with virtually no competitors. For this purpose, it has elaborated a set of colonization factors which facilitate both survival under acid exposure, motility and orientation in a highly viscous mucus layer, and adherence to epithelial surfaces. A more intimate interaction with gastric epithelia provides the basis to influence gene expression profiles as well as morphological transitions via signaling cascades or via direct activities of virulence factors. H. pylori is also one of the most genetically diverse of organisms, and variations are not only found in outer membrane adhesins, but also in two major virulence factors, the VacA cytotoxin and the cag pathogenicity island. Both factors are able to target different cell types and different interaction partners to induce a wide range of possible cellular effects. Despite the fact that H. pylori elicits a strong inflammatory response, the immune system fails to clear the infection, suggesting that immune evasion strategies are used. The mechanisms for immune evasion include the induction of a strongly polarized immune response, a modulation of phagocytosis and neutrophil function, and an inhibition of lymphocyte proliferation. Prolonged inflammation and direct action of bacterial factors may lead to impairment of gland function and eventually to carcinogenesis.
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