Amalgamation of Chlamydia pneumoniae inclusions with lipid droplets in foam cells in human atherosclerotic plaque
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Chlamydia pneumoniae (Chlamydophila pneumoniae) infect macrophages and accelerates foam cell formation in in vitro experiments, but whether this might occur in human atherosclerosis is unknown. In the present study, we examined 17 carotid artery segments, obtained by endarterectomy, in which the presence of C. pneumoniae was confirmed by both polymerase chain reaction and immunohistochemistry. Electron microscopy demonstrated the presence of structures with the appearance of elementary, reticulate and aberrant bodies of C. pneumoniae in the cytoplasm of macrophage foam cells. The volume of the cytoplasm that was free from vacuoles and lipid droplets in C. pneumoniae-infected foam cells was dramatically reduced, and a phenomenon of the amalgamation of C. pneumoniae inclusions with lipid droplets was detected. Double immunohistochemistry showed that C. pneumoniae-infected foam cells contained a large number of oxidized low-density lipoproteins. The observations provide support to the hypothesis that C. pneumoniae could affect foam cell formation in human atherosclerosis.
KeywordsAtherosclerosis Arteries Macrophages Chlamydia pneumoniae
The research was supported by the Vascular Fund, St. Vincent’s Hospital, Sydney and by School of Medicine, University of Western Sydney.
The experiments comply with the current laws of Australia.
Conflict of interest statement
We have no commercial associations (i.e. pharmaceutical stock ownership, consultancy, advisory board membership, or relevant patents) that might pose a conflict of interest. We declare that we have no conflict of interest.
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