[Helicobacter pylori, gastric inflammation and its consequences]

The stomach is an organ which is usually sterile and without lymphoid tissue. Its colonization by Helicobacter pylori leads to an important inflammatory response, gastritis. Polymorphs and macrophages are attracted and activated. Epithelial cells contribute to this innate response by the chemokines produced such as interleukin 8. The reaction observed is of Th1 type, probably inappropriate against an extra-cellular pathogen. The deleterious effect caused by oxygen free radicals is important. Two types of topographic evolution of the gastritis can be observed: antral gastritis which can lead to ulcer disease, and pangastritis which can lead to gastric carcinoma. In addition to host genetic factors, environmental factors and characteristics of the infecting strain can be involved. The maximum risk to develop a gastric cancer occurs for subjects harboring certain alleles of the interleukin 1B and H. pylori strains with the cag pathogenicity island.