Background & Aims: Investigation of the type of cellular immune response in stomach of Helicobacter felis infected mice ,and its immunopathogenic role in gastritis, and also invitro comparison of soluble Ag with heat-inactivated and urease Ag, by lymphocyte proliferation test and level of IFN-γ production. Were studied.
Materials and Methods: 15 healthy mice, C57BL/6 Strain, 6 to 8 week-old, dividing in 5 groups, each consisting of 3 mice. Four groups of mice were infected by oral administration of three dose of 3×10.7H. felis, and one groups of infected mice were killed and lymphocyte were cultured along with 3 ml of soluble Ag/well for 3 days. Then stimulation index were determined by cellular count. The assay of IFN-γ in culture supernatants were done by a sandwich ELISA. The intensity of gastritis was studied by examination of H&E-Stained histologic section and were graded to mild, moderate and severe, according to percentage of inflammatory infiltrate cells. The level of anti-Helicobacter Abs was measured by a sandwich ELISA. One group of infected mice were injected with anti- IFN- γ, and after 3 weeks were examined for level of IFN- γ, anti Helicobacter Ab, and severity of gastritis.
Results: Data showed that soluble Ag induced a proliferative response only in lymphocyte of infected mice, as stimulation index was obtained 50. In constant, heat-inactivated H.felis and urease Ag stimulated an identical response in both infected and non-infected mice. At eight weeks after infection, the cellular infiltration in gastric section were as, mononuclear 40%, plasmacell 35% and neutrophil 20%. The infected mice which received anti- IFN- γ showed a significant decrease in level of IFN-y, anti-Helicobater Ab and gastric inflammation. One and eight weeks after infection, the IFN- γ levels produced from infected mice lymphocyte were respectively 525 picogram and 755 pg/ml. In contast, noninfected mice lymphocyte had no detectable level of IFN-γ in response to Ag stimulation.
Discussion: These data demonstrate that cellular response was concomitant with Ag-specific cellular proliferation, high level of IFN-γ production and gastric inflammation. It suggests that the Helicobacter-specific Th1 response may be contributing in pathogensis of disease.