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Gastritis was induced in mice by oral administration of acetic acid 5%, a cagA positive Helicobacter pylori strain, or both. The induction of a mild gastritis by acetic acid before inoculation with H. pylori resulted in a slight but not significantly decreased colonisation rate. To study the initial stage of inflammation, the presence of gastric lymphoid and non-lymphoid cells was studied by immunohistochemistry during the first 2 weeks after induction of gastritis. Treatment with acetic acid alone or in combination with H. pylori resulted in an increase in the number of neutrophils in the mucosa and submucosa, without evident epithelial damage. The influx of neutrophils was most prominent in the mice that received a combined treatment of acetic acid and H. pylori. Macrophages were also increased in both acetic acid and acetic acid plus H. pylori-treated groups, although a different kinetic pattern was present in these groups. In mice infected with H. pylori alone, only a slight but not significant increase in neutrophils and macrophages was observed. The early presence of lymphoid aggregates in the gastric mucosa of mice in which colonisation was shown with H. pylori was remarkable. This phenomenon was not seen in control mice, in mice that received acetic acid alone or when colonisation was not shown. These data suggest that gastritis induced by a chemical agent such as acetic acid occurs by a different mechanism than gastritis induced by H. pylori and that the continued presence of H. pylori is required for local lymphocyte activation.

Local cellular immune response in the acute phase of gastritis in mice induced chemically and by Helicobacter pylori