[The implication of Chlamydia pneumoniae in damage to human aortic endotheliocytes in atherosclerosis].

A cytological technique was used to study the impressions of the aortic intima of dead patients. Endothelial cell Chlamydia pneumoniae (CP) was detected in 26 (56.5%) of 46 dead patients; the bacterium was found in the unaffected intact intimal areas in 9 (19.6%) cases. Three morphological forms of CP--inclusions, spots, and aggregates were described. The whole life cycle of CP and the specific features of disintegration of the host cell--the endothelium were observed. CP leads to extensive infection and aponecrotic death of all types of endothelial cells above the fatty streaks and plaques. Focal chlamydial destruction of an endothelial layer results in intimal surface erosion and thrombogenesis. An inflammatory response to damaged endothelial cells may be responsible for the initiation and progression of atherosclerosis and plaque destabilization.