Abstract
Recently, Chlamydia pneumoniae (C pneumoniae) has been noteworthy to be linked to an atherosclerotic disease and clinical evidence that C pneumoniae infection contributes to atherosclerosis is accumulating. We clarified the detail distribution of C pneumoniae infection in the atherosclerotic carotid artery by im-munohistochemistry and electron microscopy.
Twenty-seven specimens of carotid atheromatous plaque were obtained during carotid endarterectomy in 26 patients with severe carotid artery stenosis. Immunoreactivity for the C pneumoniae-specific antigen was observed in 55% of patients, and intense immunoreactivity was observed in 35% of patients. C pneumoniae infection was observed in endothelial cells, macrophages and smooth muscle cells that had migrated into the atheromatous plaque, as well as in smooth muscle cells and small arteries in the media underlying the atheromatous plaques. C pneumoniae infection was most prominently observed in smooth muscle cells. In electron microscopy, a pear-shaped elementary body of C pneumoniae was observed.
Macrophages in the intima produce some cytokines and growth factors, and elicit migration of smooth muscle cells from the media to the intima as well as an inflammatory response which subsequently leads to atherosclerosis progression. Chronic infection of C pneumoniae may enhance the proliferative and inflammatory processes of atherosclerosis by inducing some cytokines and lipoproteins through activation of transcription factors such as nuclear factor (NF)-kB.
