Role of Chlamydia pneumoniae-infected macrophages in atherosclerosis developments of the carotid artery

Chlamydia pneumoniae (C. pneumoniae) infection has been recently accepted as an important cause of atherosclerosis. However, the precise mechanisms remain unclear. The present study was aimed to clarify the distribution link among C. pneumoniae , chlamydial HSP 60, and activated macrophages. Atheromatous carotid plaques were obtained from 40 consecutive carotid endarterectomies (CEA). The specimens were prepared for HE and elastica-van Gieson staining. Parallel sections were stained immunocytochemically with monoclonal antibodies for a C. pneumoniae -specific antigen, chlamydial HSP 60, activated macrophages, and smooth muscle cells. Immunoreactivity for the C. pneumoniae-specific antigen was observed within the endothelial cells, activated macrophages, and smooth muscle cells in 36 of 40 specimens (90%). Chlamydial HSP 60 was found in all specimens positive for the C. pneumoniae-specific antigen, and mainly co-localized with the C. pneumoniae -specific antigen within the activated macrophages. The present results suggest that C. pneumoniae is a key microbial organ that causes atheroma developments in the carotid artery. Chlamydia pneumoniae -infected macrophages may come into the arterial intima and mediate inflammatory and autoimmune processes through the production of chlamydial HSP 60, leading to atherosclerosis.