Pathogenesis of Helicobacter pylori infection

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Abstract
Five years after publication of the complete genome sequence of Helicobacter pylori, research interest is shifting from the descriptive association of virulence factors with clinical outcome in infected patients to the molecular mechanisms of virulence factor action. This is particularly noticeable for VacA and CagA, for both of which detailed understanding of the interaction with host signalling pathways has accumulated over the last year. The role of H. pylori Lewis antigens for clinical outcome was further substantiated. Various strategies of H. pylori to fool or evade the human immune system are described, which all lead to the dysfunction of specific compartments of the host cellular immune system. Finally, a number of animal models indicate that inflammation is a key factor for gastric carcinogenesis, which is finally supported by a large prospective study identifying corpus atrophy and intestinal metaplasia as precancerous conditions.