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Title: Decreased expression of liver X receptor-α in macrophages infected with chlamydia pneumoniae in human atherosclerotic arteries in situ
Authors: Bobryshev, Y.V.
Orekhov, A.N.
Killingsworth, M.C.
Lu, J. 
Keywords: Arteries
Chlamydia pneumoniae
Foam cells
Issue Date: Aug-2011
Citation: Bobryshev, Y.V., Orekhov, A.N., Killingsworth, M.C., Lu, J. (2011-08). Decreased expression of liver X receptor-α in macrophages infected with chlamydia pneumoniae in human atherosclerotic arteries in situ. Journal of Innate Immunity 3 (5) : 483-494. ScholarBank@NUS Repository.
Abstract: In in vitro experiments, Chlamydia pneumoniae has been shown to infect macrophages and to accelerate foam cell formation. It has been hypothesized that the C. pneumoniae infection affects foam cell formation by suppressing the expression of liver X receptors (LXR), but whether such an event occurs in human atherosclerosis is not known. In this study we examined carotid artery segments, obtained by endarterectomy, in which the presence of C. pneumoniae was confirmed by both polymerase chain reaction and immunohistochemistry. The expression of LXR-α in macrophages infected with C. pneumoniae and macrophages that were not infected was compared using a quantitative immunohistochemical analysis. The analysis revealed a 2.2-fold reduction in the expression of LXR-α in C. pneumoniae-infected cells around the lipid cores in atherosclerotic plaques. In the cytoplasm of laser-capture microdissected cells that were immunopositive for C. pneumoniae, electron microscopy demonstrated the presence of structures with the appearance of elementary, reticulate and aberrant bodies of C. pneumoniae. We conclude that LXR-α expression is reduced in C. pneumoniae-infected macrophages in human atherosclerotic lesions which supports the hypothesis that C. pneumoniae infection might suppress LXR expression in macrophages transforming into foam cells. © 2011 S. Karger AG, Basel.
Source Title: Journal of Innate Immunity
ISSN: 1662811X
DOI: 10.1159/000327522
Appears in Collections:Staff Publications

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