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 in | The Journal of infectious diseases Vol. 180; no. 3; pp. 780 - 790 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Chicago, IL
The University of Chicago Press
01.09.1999
University of Chicago Press Oxford University Press |
Subjects | |
Online Access | Get full text |
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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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Bibliography: | istex:BD3FF7FE590ED4FA73D65A96E893D495ED9CCF42 ark:/67375/HXZ-5PVB06X6-1 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-1899 1537-6613 |
DOI: | 10.1086/314931 |