Abstract
Although virtually everyone who is infected with Helicobacter pylori will display chronic active gastritis, such people are generally free of other symptoms, and only a minority of infected individuals develop more severe disease and overt symptoms. This has been ascribed both to differences among bacterial isolates, most notably in the cag pathogenicity island1, for which CagA is a marker, and to differences in the host response to infection2,3. Interaction of the bacteria with gastric epithelial cells leads to epithelial secretion of interleukin 6 (IL-6), IL-8, and other innate mediators which are important in recruiting neutrophils to the gastric compartment4–6. The presence of significant numbers of lymphocytes in the inflamed gastric tissue of H. pylori-infected individuals suggests that the adaptive immune response may also contribute to Helicobacter-associated gastritis.
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Nedrud, J.G., Mohammadi, M., Blanchard, T., Redline, R., Czinn, S.J. (1998). Th1/Th2 lymphocyte responses in Helicobacter infections. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4882-5_13
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DOI: https://doi.org/10.1007/978-94-011-4882-5_13
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