IL-9 aggravates the development of atherosclerosis in ApoE-/-mice

Zhang Wencai Tang Tingting Nie Daan Wen Shuang Jia Chenping Zhu Zhengfeng Xia Ni Nie Shaofang Zhou Sufeng Jiao Jiao Dong Wenyong Lv Bingjie Xu Tongjie Sun Bing Lu Yuzhi Li Yuanyuan Cheng Longxian Liao Yu-Hua Cheng Xiang · 2015

阅读量：116

动脉粥样硬化

9月-

炎症

血管内皮细胞粘附分子-1

期刊名称：

Cardiovascular Research 2015 年 106 卷 3 期

发表日期：

2015.06.01

摘要：

Aims: Recently, interleukin (IL)-9 was found to be involved in the pathogenesis of many inflammatory diseases. Here, we tested whether IL-9 was related to atherosclerosis and investigated the underlying mechanisms. Methods and results: IL-9R was expressed in mouse aortic endothelial cells (MAECs) and aortic tissues, and IL-9 levels were elevated in plasma and aortic arches in Apolipoprotein E-deficient (ApoE-/-) mice. ApoE-/- mice fed a western diet for 10 weeks were administered recombinant mouse IL-9 (rIL-9) or anti-IL-9 neutralizing monoclonal antibody (mAb). Mice treated with rIL-9 developed markedly larger plaques in both the aorta and aortic root. Immunohistochemical studies demonstrated increases in both vascular endothelial adhesion molecule-1 (VCAM-1) expression and the infiltration of inflammatory cells, including T cells and macrophages, in plaques. However, treatment with the anti-IL-9 mAb caused the opposite effect. The administration of rIL-9 did not affect the splenic T cell or peripheral monocyte subsets. Meanwhile, IL-9 induced VCAM-1 expression in MAECs mainly via a STAT3-dependent pathway, consequently increasing monocyte-endothelial adhesion. Moreover, treatment with anti-VCAM-1 mAb partially abrogated the IL-9-induced increase in plaque area. In addition, CD4