Nuclear factor-κB activation in endothelium by Chlamydia pneumoniae without active infection

被引：14

作者：

Baer, JT

du Laney, TV

Wyrick, PB

McCain, AS

Fischer, TA

Merricks, EP

Baldwin, AS

Nichols, TC

机构：

[1] Univ N Carolina, Dept Pathol & Lab Med, Francis Owen Blood Res Lab, Chapel Hill, NC 27516 USA

[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27516 USA

[3] Univ N Carolina, Dept Biol, Chapel Hill, NC 27516 USA

[4] Univ N Carolina, Sch Med, Chapel Hill, NC 27516 USA

来源：

JOURNAL OF INFECTIOUS DISEASES | 2003年 / 188卷 / 08期

关键词：

D O I：

10.1086/378564

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Causative molecular mechanisms accounting for the potential link between Chlamydia pneumoniae and atherosclerosis are unknown. Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)-kappaB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IkappaB super-repressor, an NF-kappaB-specific inhibitor. Live bacteria are not necessary for the activation of endothelial NF-kappaB, and C. pneumoniae may contribute to atherogenesis without active infection.

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收藏

页码：1094 / 1097

页数：4

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