Analysis of progression of atherosclerosis after Kawasaki disease by coronary arteritis mouse model

Nod 1配体诱导小鼠川崎样冠状动脉炎在ApoE KO小鼠中通过施用Nod 1配体发生冠状动脉炎后，评估动脉粥样硬化的进展。冠状动脉炎诱导的ApoE基因敲除小鼠的动脉粥样硬化进展比未诱导的ApoE基因敲除小鼠。冠状动脉内细胞因子和趋化因子如Ccl 5和Cxcl 16的产生是导致冠状动脉病变进展的主要原因。此外，Nod 1/ApoE双基因敲除小鼠的动脉粥样硬化进展比ApoE KO小鼠慢。这些结果提示，可能由川崎引起的先天免疫配体参与了动脉粥样硬化的发生发展。

Nod1 ligand induces Kawasaki disease-like coronary arteritis in mice. After coronary arteritis developed in ApoE KO mice by administration of Nod1 ligand, the progression of atherosclerosis was assessed. Atherosclerosis in coronary artritis-induced ApoE KO mice was progressed more than in not induced ApoE KO mice. And the progression was caused by production of cytokines and chemokines like Ccl5 and Cxcl16 in coronary artery. Furthermore, atherosclerosis in Nod1/ApoE double knockout mice progressed more slowly than that in ApoE KO mice. These finginds suggested that innate immune ligands possibly caused by Kawasaki disease would progress atherosclerosis.