Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice
Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice作者机构：Department of Immunology Shandong University School of Medicine and Jinan China Key Laboratory of Cardiovascular Remodeling and Function Research Qilu Hospital Shandong University .linan China
出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)
年 卷 期：2013年第10卷第4期
页 面：338-348页
核心收录：
学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 081704[工学-应用化学] 07[理学] 08[工学] 0817[工学-化学工程与技术]
基 金：Our study was supported by the National '973' Program of China (2011CB503900) the National Natural Science Foundation of China (30628015 30700729 and 30872309) and Natural Science foundation of Shandong (Z2008C02)
主 题：atherosclerosis mice plaque rupture Th1 Th17
摘 要：Considerable evidence indicates that type 1 T helper （Th 1）- and Th 17-mediated immune responses promote the formation of atherosclerotic plaques while that CD4＋CD25＋Foxp3＋ regulatory T cells （Tregs） have a protective effect. However, the functions of diverse CD4＋ lymphocyte subsets in plaque rupture remain poorly understood because of a shortage of satisfactory plaque rupture models. Here, we established a murine model of atherosclerotic plaque rupture using a high-fat diet and collar placement on the carotid artery, and triggered plaque rupture by short-term stimulation with a combination of lipopolysaccharide, phenylephrine injection and cold in apolipoprotein E-knockout （ApoE-/-） mice. We investigated the associations between Thl cells, Th17 cells and Tregs and plaque rupture by PCR, flow cytometry, ELISA and immunohistochemistry. In total, 75% （18/24） of vulnerable plaques, but no stable plaques, showed rupture characteristics. The proportion of Th17 cells was increased among splenocytes after treatment, but the changes in the levels of Thl ceils and Tregs were not related to rupture. Furthermore, the treatment resulted in high levels of interleukin- 17 （IL-17） in the serum and in the region of plaque rupture, in vitro, IL-17 increased the level of apoptosis, a major factor associated with plaque rupture, in cultured murine vascular smooth muscle cells. Th17 cells and IL-17 may be involved in the disruption of vulnerable plaques triggered by short-term stimulation with lipopolysaccharide, phenylephrine injection and cold in ApoE-/-mice.
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