Histological and ultrastructural findings suggesting an initiating role for Chlamydia pneumoniae in the pathogenesis of atherosclerosis.

Abstract

AIMS: An association between Chlamydia pneumoniae and atherosclerosis is now well established. The finding of C. pneumoniae in atherosclerotic lesions has led to the hypothesis that this organism may have an aetiological role in atherogenesis. The implications of such a concept are enormous, but to date the pathological features of the lesion have not been examined in the light of this new hypothesis. This study was designed to determine the pathological basis of the association between C.pneumoniae and atherosclerotic lesions. METHODS: The pathological features of 50 atherosclerotic lesions from 50 different patients, in which C.pneumoniae had been demonstrated by immunocytochemistry and PCR techniques, were examined using light and electron microscopy techniques. In 20 cases the lesions were fatty streaks, 20 were fibro-atheroma lesions, and 10 were advanced, complicated lesions. RESULTS: Intimal smooth-muscle cells infected with C. pneumoniae exhibit vacuolation, loss of myofilaments, an increase in lipid, rupture and fragmentation. Macrophages phagocytose these muscle cell fragments, lipid and C. pneumoniae. Large numbers of extracellular C. pneumoniae organisms were identified in the central necrotic core, in areas of fibrosis, in areas of fragmentation of the internal elastic lamina, and in ceroid bodies. Neither pathological changes nor organisms were seen in the endothelium. CONCLUSIONS : C. pneumoniae infection of intimal smooth&hypen; muscle cells is accompanied by cytoplasmic alterations and damage. The fatty streak appears to be formed by a macrophage response to this muscle damage. C. pneumoniae is found in early, mature and advanced lesions. This is the first study of the pathology of atherosclerosis suggesting that the lesion be interpreted as an infective chlamydial granuloma.