Chlamydia pneumoniae infection increases adherence of mouse macrophages to mouse endothelial cells in vitro and to aortas ex vivo.
Chlamydia pneumoniae infection increases adherence of mouse macrophages to mouse endothelial cells in vitro and to aortas ex vivo.
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肺炎衣原体感染增加小鼠巨噬细胞在体外对小鼠内皮细胞和离体主动脉的粘附。
DOI：
10.1128/iai.01267-07
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发表时间：
2008
影响因子：
3.1
通讯作者：
Kuo,Cho-Chou
中科院分区：
文献类型：
--
作者：
Takaoka,Naohisa;Campbell,LeeAnn;Lee,Amy;Rosenfeld,MichaelE;Kuo,Cho-Chou
单核/巨噬细胞与内皮细胞之间的相互作用在动脉粥样硬化的发病机制中起着重要作用，单核细胞与动脉内皮细胞的黏附是动脉粥样硬化形成的早期事件之一。本研究利用绿色荧光蛋白(GFP)转基因小鼠的腹膜巨噬细胞，分析肺炎衣原体感染对GFP-巨噬细胞与体外培养的小鼠内皮细胞及正常和高脂小鼠的主动脉黏附的影响。体外研究表明，肺炎衣原体感染的GFP-巨噬细胞对内皮细胞的黏附能力强于未感染的巨噬细胞，GFP-巨噬细胞对感染的内皮细胞的黏附能力强于未感染的内皮细胞。体外研究表明，肺炎衣原体感染的巨噬细胞对正常和高脂C57BL/6J小鼠及载脂蛋白E(ApoE)缺陷小鼠的主动脉黏附能力均好于未感染的巨噬细胞。相反，细胞间黏附分子-1(ICAM-1)基因敲除的小鼠，感染肺炎链球菌的巨噬细胞与主动脉的黏附并未增强，提示ICAM-1对肺炎链球菌感染的巨噬细胞黏附血管内皮细胞的激活至关重要。综上所述，本研究明确了肺炎衣原体通过促进单核巨噬细胞与动脉粥样硬化病变形成部位的内皮细胞的黏附而促进动脉粥样硬化进展的归巢机制。
Interactions between monocytes/macrophages and endothelial cells play an important role in the pathogenesis of atherosclerosis, and the adherence of monocytes to the arterial endothelium is one of the early events in atherogenesis. In the present study, peritoneal macrophages harvested from green fluorescent protein (GFP) transgenic mice were used to analyze howChlamydia pneumoniaeinfection affects the adherence of GFP-macrophages to mouse endothelial cells in vitro and to the aorta from normolipidemic and hyperlipidemic mice ex vivo. In vitro studies showed thatC.pneumoniae-infected GFP-macrophages adhered better than uninfected macrophages to endothelial cells and GFP-macrophages adhered better to infected than uninfected endothelial cells. The ex vivo studies showed thatC.pneumoniae-infected macrophages adhered better than uninfected macrophages to aortas from both normolipidemic and hyperlipidemic C57BL/6J mice and apolipoprotein E (ApoE)-deficient mice. In contrast, adherence ofC.pneumoniae-infected macrophages to the aortas of intercellular adhesion molecule 1 (ICAM-1) knockout mice was not enhanced, suggesting that ICAM-1 is crucial for activation of the adherence ofC.pneumoniae-infected macrophages to the endothelium. In conclusion, the present study defined a homing mechanism by whichC.pneumoniaepromotes the adherence of mononuclear phagocytes to the endothelium at the site of atherosclerotic lesion formation to promote the progression of atherosclerosis.