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Abstract

It is now clear that Helicobacter pylori, one of the commonest bacterial infections of man, is the causative agent of chronic gastritis. Volunteer, treatment and animal model studies all implicate this organism as the aetiological agent inducing gastric inflammation. Many infected subjects remain asymptomatic. However, the increasing importance of H. pylori in peptic ulcer disease1, gastric adenocarcinoma (Chapter 2 of this volume) and gastric MALT lymphoma2,3 stresses the relevance of this bacterial infection to gastroduodenal disease. Whilst several potential bacterial pathogenic factors have been described in the chapter by Blaser (Chapter 4) in this volume, our understanding of the role of H. pylori in the pathogenesis of gastroduodenal disease is still limited. The local immune response to the organism, characterized by infiltration of plasma cells, neutrophils, lymphocytes and monocytes, may be an important factor in the pathogenesis of H. pylori-associated gastroduodenal lesions. Variations in host responses to infection determined by immune response genes may be critical in determining the extent of H. pylori-induced mucosal injury. There is also increasing evidence that inflammatory responses may reflect strain variation in H. pylori 4,5.

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Crabtree, J., Wyatt, J. (1993). Host responses. In: Northfield, T., Mendall, M., Goggin, P.M. (eds) Helicobacter pylori Infection. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2216-0_5

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  • DOI: https://doi.org/10.1007/978-94-011-2216-0_5

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