抄録
Atherosclerosis is closely related to chronic infection. In the present study, we evaluated atherogenesis by gastric infection with Helicobacter pylori (H. pylori) in atherosclerosis-prone apoe+/-ldlr+/- mice. Six- week- old male apoe+/-ldlr+/- mice infected by H. pylori and apoe+/-ldlr+/- control mice were fed with a high cholesterol diet (1%). Eight weeks after the confirmation of infection, the extent of atherosclerosis, anti heat shock protein 60 of H. pylori (Hp-HSP60) serum titers, and the cellular immune responses against Hp-HSP60 were evaluated. Atherosclerosis was promoted by a Th1-mediated reaction against Hp-HSP60, accompanied by production of IFN-γ and IL-12, and mRNA expression of T-bet in the H. pylori -infected apoe+/-ldlr+/- mice. The over-expressed of HSP60 in stressed endothelial cells could be cross-recognized by T cells against Hp-HSP60 and contributed to the atherosclerosis. This mouse model would be useful for analyzing immunological mechanisms of atherogenesis.
