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J Infect Dis. 1999 Sep;180(3):780-90.

Cellular oxidation of low-density lipoprotein by Chlamydia pneumoniae.

Author information

1
Department of Medical Microbiology and Immunology, Universityof Wisconsin Medical School, Madison WI 53706, USA.

Abstract

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.

PMID:
10438367
DOI:
10.1086/314931
[Indexed for MEDLINE]

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