Tumor necrosis factor receptor superfamily members 1a and 1b contribute to exacerbation of atherosclerosis by Chlamydia pneumoniae in mice

被引:6
|
作者
Zafiratos, Mark T. [1 ]
Cottrell, Jonathan T. [2 ]
Manam, Srikanth [3 ]
Henderson, Kyle K. [2 ]
Ramsey, Kyle H. [2 ,3 ]
Murthy, Ashlesh K. [3 ]
机构
[1] Midwestern Univ, Coll Hlth Sci, Downers Grove, IL 60515 USA
[2] Midwestern Univ, Chicago Coll Osteopath Med, Downers Grove, IL 60515 USA
[3] Midwestern Univ, Coll Vet Med, Glendale, AZ 85308 USA
基金
美国国家卫生研究院;
关键词
Chlamydia pneumoniae; Atherosclerosis; Pathogenesis; Tumor necrosis factor; Tumor necrosis factor receptor 1; Tumor necrosis factor receptor 2; CD8(+) T-CELLS; TARGET; TNFR2;
D O I
10.1016/j.micinf.2018.09.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The host immune responses that mediate Chlamydia-induced chronic disease sequelae are incompletely understood. The role of TNF-alpha, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2), in Chlamydia pneumoniae (CPN)-induced atherosclerosis was studied using the high-fat diet-fed male C57BL/6J mouse model. Following intranasal CPN infection, TNF-alpha knockout (KO), TNFR1 KO, TNFR2 KO, and TNFR 1/2 double-knockout, displayed comparable serum anti-chlamydial antibody response, splenic antigen-specific cytokine response, and serum cholesterol profiles compared to wild type (WT) animals. However, atherosclerotic pathology in each CPN-infected KO mouse group was reduced significantly compared to WT mice, suggesting that both TNFR1 and TNFR2 promote CPN-induced atherosclerosis. (C) 2018 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:104 / 108
页数:5
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