Chlamydia pneumoniae and atherosclerosis

Chlamydia pneumoniae (C. pneumoniae) is a common respiratory pathogen. Many reports have documented the presence of C. pneumoniae in atheromatous coronary arteries, aorta, carotid arteries, and peripheral arteries using a variety of techniques. There is clear experimental evidence that C. pneumoniae can infect macrophages, endothelial cells, smooth muscle cells, and induce the formation of foam cells. Evidence from basic research and epidemiologic studies suggest that C. pneumoniae can induce macrophage foam cell formation by dysregulating native LDL uptake or metabolism (or both). Relatively small, secondary prevention studies, have suggested that antibiotic therapy might reduce monocyte activation and C. pneumoniae antibody titers, reduce inflammatory markers and possibly reduce adverse cardiovascular events. It is possible that C. pneumoniae enhances atherogenesis by causing inflammation and eliciting immune responses and may be one of the factors contributing to this multifactorial disease process.