Porphyromonas gingivalis accelerates inflammatory atherosclerosis in the innominate artery of ApoE deficient mice

被引:80
作者
Hayashi, Chie [1 ]
Viereck, Jason [2 ]
Hua, Ning [2 ]
Phinikaridou, Alkystis [2 ]
Madrigal, Andres G. [1 ]
Gibson, Frank C., III [1 ]
Hamilton, James A. [2 ,4 ]
Genco, Caroline A. [1 ,3 ]
机构
[1] Boston Univ, Sch Med, Dept Med, Infect Dis Sect, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Physiol & Biophys, Boston, MA 02118 USA
[3] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA
[4] Boston Univ, Dept Biomed Engn, Coll Engn, Boston, MA 02118 USA
基金
美国国家卫生研究院;
关键词
Atherosclerosis; Inflammation; P; gingivalis; Infection; Innominate artery; MRI; APOLIPOPROTEIN E-DEFICIENT; ORAL BONE LOSS; PLAQUE RUPTURE; PERIODONTAL-DISEASE; ENDOTHELIAL DYSFUNCTION; ATHEROMATOUS PLAQUES; MURINE MODELS; RABBIT MODEL; MOUSE; INFECTION;
D O I
10.1016/j.atherosclerosis.2010.12.009
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: Studies in humans support a role for the oral pathogen Porphyromonas gingivalis in the development of inflammatory atherosclerosis. The goal of this study was to determine if P. gingivalis infection accelerates inflammation and atherosclerosis in the innominate artery of mice, an artery which has been reported to exhibit many features of human atherosclerotic disease, including plaque rupture. Methods and results: Apolipoprotein E-deficient (ApoE(-/-)) mice were orally infected with P. gingivalis, and magnetic resonance imaging (MRI) was used to monitor the progression of atherosclerosis in live mice. P. gingivalis infected mice exhibited a statistically significant increase in atherosclerotic plaque in the innominate artery as compared to uninfected mice. Polarized light microscopy and immunohistochemistry revealed that the innominate arteries of infected mice had increased lipids, macrophages and T cells as compared to uninfected mice. Increases in plaque, total cholesterol esters and cholesterol monohydrate crystals, macrophages, and T cells were prevented by immunization with heat-killed P. gingivalis prior to pathogen exposure. Conclusions: These are the first studies to demonstrate progression of inflammatory plaque accumulation in the innominate arteries by in vivo MRI analysis following pathogen exposure, and to document protection from plaque progression in the innominate artery via immunization. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:52 / 59
页数:8
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