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Contempo 1999 |

Chlamydia pneumoniae and Atherosclerosis

Allan Shor, MMed; James I. Phillips, PhD
JAMA. 1999;282(21):2071-2073. doi:10.1001/jama.282.21.2071.
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Atherosclerosis is a major cause of stroke, coronary heart disease, peripheral vascular disease, and aortic aneurysm. Because of the prevalence and importance of these diseases, atherosclerotic lesions within arteries have been extensively studied.1,2 While many risk factors have been identified,1,2 the mechanism by which the lesions are formed remains unknown. The most popular concept is that the endothelium lining the lumen of the artery becomes damaged. This damage alters the properties of the endothelium and leads to a cascade of events culminating in fibrosis, necrosis, lipid accumulation, and eventually calcification. There have been several candidates forwarded as putative initiators of endothelial injury including microorganisms.1 Recent studies have shown an association between an obligate intracellular bacterium, Chlamydia pneumoniae, and atherosclerosis.3,4

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Figure 1. Photomicrograph of an Early Atherosclerotic Lesion of the Aorta Positive for Chlamydia pneumoniae by Polymerase Chain Reaction
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The smooth muscle cells are histochemically stained for smooth muscle actin (brown) and counterstained with hematoxylin to show evidence of vacuolation. A indicates smooth muscle cell actin; V, vacuoles (original magnification × 400).
Figure 2. Transmission Electron Micrograph of Smooth Muscle Cells in an Early Atherosclerotic Lesion of the Aorta Positive for Chlamydia pneumoniae by Polymerase Chain Reaction
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Left, one smooth muscle cell contains vacuoles (V) and C pneumoniae elementary bodies (arrowhead); the other is fragmenting. A indicates actin filaments. Right, macrophage pseudopodia (P) in contact with a fragment of smooth muscle cell (SMC) containing C pneumoniae (arrowheads). (Reproduced with permission from the Cardiovascular Journal of Southern Africa.38)

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