Cellular oxidation of low-density lipoprotein by Chlamydia pneumoniae.
A spectrum of clinical and epidemiologic studies implicate infectious agents, including Chlamydia pneumoniae, in the pathogenesis of atherosclerosis. The complexity of atherosclerotic disease necessitates examining the role of infection in the context of defined risk factors, such as high levels of native low-density lipoprotein (LDL). Although native LDL does not have atherogenic properties, cellular oxidation of LDL alters the lipoprotein into a highly atherogenic form. In this report, C. pneumoniae and chlamydial hsp60, an inflammatory antigen that was recently localized to atheromas, were found to induce cellular oxidation of LDL. These data provide initial evidence that an infectious agent can render LDL atherogenic and suggest a mechanism whereby C. pneumoniae may promote atheroma development.
Kalayoglu
M V
MV
Department of Medical Microbiology and Immunology, Universityof Wisconsin Medical School, Madison WI 53706, USA.
Hoerneman
B
B
LaVerda
D
D
Morrison
S G
SG
Morrison
R P
RP
Byrne
G I
GI
D001161:Arteriosclerosis / Q000209:etiology; D002478:Cells, Cultured; D018834:Chaperonin 60 / Q000378:metabolism; D016993:Chlamydophila pneumoniae / Q000378:metabolism*; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood* / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D009000:Monocytes / Q000187:drug effects / Q000382:microbiology / Q000502:physiology; D012307:Risk Factors; D012867:Skin / Q000166:cytology / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000494:pharmacology
D018834:Chaperonin 60; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; C099252:oxidized low density lipoprotein; D014810:Vitamin E; D008315:Malondialdehyde