Endothelial Chlamydia pneumoniae infection promotes oxidation of LDL

被引：22

作者：

Dittrich, R ^{[1
]}

Dragonas, C

Mueller, A

Maltaris, T

Rupp, J

Beckmann, MW

Maass, M

机构：

[1] Univ Erlangen Nurnberg, Dept Obstet & Gynecol, Erlangen, Germany

[2] Med Univ Lubeck, Inst Med Microbiol & Hyg, D-23538 Lubeck, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 319卷 / 02期

关键词：

Chlamydia pneumoniae; infection; atherosclerosis; LDL oxidation; endothelium; HUVEC;

D O I：

10.1016/j.bbrc.2004.04.192

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The bacterium Chlamydia pneumoniae chronically infects atheromatous lesions and is linked to atherosclerosis by modifying inflammation, proliferation, and the lipid metabolism of blood monocytes. As continuous LDL modification in the vascular intima is crucial for atherogenesis we investigated the impact of endothelial infection on LDL oxidation. HUVEC were infected with a vascular C pneumoniae strain. Supernatants of infected cells but not cell lysates increased lipid peroxidation products (6.44 vs 6.14 nmol/ml, p < 0.05) as determined by thiobarbituric acid reacting substances assay. Moreover, supernatants rendered human LDL more susceptible to oxidation as shown in a copper-ion catalysed LDL oxidation assay by a 16% reduction of LDL resistance against pro-oxidative stimuli (p < 0.05). Chlamydial infection of vascular endothelial cells releases acellular components that convert LDL to its proatherogenic form and reduce its resistance against oxidation. Foci of chronic endothelial chlamydial infection may thus continuously contribute to the dysregulated lipid metabolism that promotes atherogenesis. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：501 / 505

页数：5

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