Endothelial Chlamydia pneumoniae infection promotes oxidation of LDL.
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.
Dittrich
Ralf
R
University of Erlangen/Nuremberg, Department of Obstetrics and Gynecology, Erlangen, Germany. ralf.dittrich@gyn.imed.uni-erlangen.de
Dragonas
Charalampos
C
Mueller
Andreas
A
Maltaris
Theodoros
T
Rupp
Jan
J
Beckmann
Matthias W
MW
Maass
Matthias
M
D002384:Catalysis; D002460:Cell Line; D002690:Chlamydia Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016993:Chlamydophila pneumoniae / Q000302:isolation & purification*; D003300:Copper / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism*; D010084:Oxidation-Reduction; D017392:Thiobarbituric Acid Reactive Substances
D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; D003300:Copper