ABSTRACTHelicobacter pylori, Gramnegative bacteria discovered by Warren and Marshall [1] in 1983, colonise the stomachs of up to 50% of the humans in developed countries and 90% adult people in the developing world. The majority of H. pylori-infected individuals will be asymptomatic although the infections appear to be life lasting. In 15-20% infected persons, H. pylori bacteria induce chronic dyspepsia, duodenal and gastric ulcers and they are a risk factor for gastric cancer. Twenty years’ intensive studies yielded several descriptions of the association of immune reactions to bacterial virulence factors with extraordinarily differentiated outcome of H. pylori infections and gastric diseases caused by these pathogens. Presently a lot of research has focused on the understanding of the bacteria-host interactions resulting in chronic inflammation being a key factor determining the clinical presentations. A significant progress of the knowledge on the structure and functioning of the gut associated lymphocyte tissues opens new perspectives for exploring the responses of immunocompetent cells to bacterial proteins and non protein antigens, expressed by the changes in the surface receptors, migration to gastric mucosa, cytokine signalling. The open question is the role of antigenic mimicry in the pathogenesis of H. pylori infections as well as the immune evasion allowing bacteria to survive in infected hosts despite vigorous humoral and cellular immune responses. Much effort has been made to identify host genetic factors posing a risk of the development of gastric cancer. Because the treatment of H. pylori infections is complicated and not always successful, the strategy which has been suggested for control of H. pylori- associated gastric ulceration and cancer is vaccination.
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