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...

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Published inThe Journal of infectious diseases Vol. 180; no. 3; pp. 780 - 790
Main Authors Kalayoglu, Murat V., Hoerneman, Brian, LaVerda, David, Morrison, Sandra G., Morrison, Richard P., Byrne, Gerald I.
Format Journal Article
LanguageEnglish
Published Chicago, IL The University of Chicago Press 01.09.1999
University of Chicago Press
Oxford University Press
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Summary: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.
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ISSN:0022-1899
1537-6613
DOI:10.1086/314931