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

冠状动脉炎小鼠模型分析川崎病后动脉粥样硬化的进展

• 批准号: 24791071
• 负责人: TANAKA Tamami
• 金额: $ 2.66万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24791071/
• 关键词: 川崎病; 自然免疫; 動脈硬化

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.

Nod1配体诱导小鼠川崎病样冠脉炎在ApoE KO小鼠通过注射Nod1配体发生冠脉炎后，评估了动脉粥样硬化的进展。冠状动脉炎症诱导的载脂蛋白E-KO小鼠较未诱导的载脂蛋白E-KO小鼠动脉粥样硬化进展更严重。进展是由冠状动脉产生细胞因子和趋化因子如CCL5和CxCl16引起的。此外，Nod1/ApoE双基因敲除小鼠的动脉粥样硬化进展慢于ApoE KO小鼠。这些指征表明，可能由川崎病引起的先天免疫配体可能会导致动脉粥样硬化的进展。