Chlamydia pneumoniaein foci of “early” calcification of the tunica media in arteriosclerotic arteries: an incidental presence?

Abstract

Only a few previous works investigated the involvement of Chlamydia pneumoniae (Chlamydophila pneumoniae) in arterial calcification. The present study investigated a possible association between C. pneumoniae and medial calcification. Carotid artery segments obtained by endarterectomy from 60 patients were examined by PCR and immunohistochemistry to identify the presence of C. pneumoniae. Arterial specimens showing double-positive (n = 17), double-negative (n = 22), and single-positive results (n = 21) were further analyzed by a combination of histology, immunohistochemistry, and electron microscopy. Medial calcification occurred in 10 of 17 (58.8%) C. pneumoniae double-positive arterial specimens, but no medial calcification was observed in any of 22 C. pneumoniae double-negative arterial specimens. Electron microscopy indicated C. pneumoniae in smooth muscle cells (SMCs) in foci of medial calcification. Medial SMCs showing damage to the cytoplasm and basement membrane contained the structures with the appearance of elementary, reticulate, and aberrant bodies of C. pneumoniae. The presence of C. pneumoniae in SMCs was confirmed by electron-microscopic immunocytochemistry. In the extracellular matrix, calcification was observed in C. pneumoniae aberrant bodies that exited the SMCs. The findings offer a new hypothesis of arterial calcification: they suggest that C. pneumoniae infection of medial SMCs may be associated with the pathophysiological events of arteriosclerotic calcification of the tunica media.

Allograft Vasculopathy Versus Atherosclerosis

“…This first suggestion of infection was observed in the 1970s on noting the presence of monoclonal SMCs. 22 Observed presence of Chlamydia in foci of tunica media calcifications 23 suggested the hypothesis of infection of SMCs by Chlamydia as the initiating point in atherosclerosis. Another theory is the observed double-infection by both Chlamydia and CMV causing a synergistic increase in inflammatory response and perhaps speeding atherosclerosis progression.…”

Decreased Expression of Liver X Receptor-α in Macrophages Infected with <i>Chlamydia pneumoniae</i> in Human Atherosclerotic Arteries in situ

“…Archival tissue specimens, some characteristics of which were reported previously [15,16,44] , were used in the present study and represented carotid artery tissues obtained by endarterectomy from 39 patients whose ages ranged from 52 to 75 years (24 males and 15 females) [15] . The study was carried out in accordance with the principles outlined in the Helsinki Declaration and informed consent was obtained from each patient [15] .…”

The prospective association of Chlamydia pneumoniae and four other pathogens with development of coronary artery calcium: The Multi-Ethnic Study of Atherosclerosis (MESA)

“…Several studies have suggested that infection may play a role in the development of calcification (10, 11). Pathogens such as Chlamydia pneumoniae infect human macrophages, endothelial cells and arterial smooth muscle cells (12), and induce production of cytokines and matrix metalloproteinases, thus potentially contributing to calcification (11, 13, 14).…”

“…Pathogens such as Chlamydia pneumoniae infect human macrophages, endothelial cells and arterial smooth muscle cells (12), and induce production of cytokines and matrix metalloproteinases, thus potentially contributing to calcification (11, 13, 14). An intense inflammatory process by pathogen infection may result in debris of cellular membranes of the bacteria and host cells, creating a substrate for calcium deposition (15).…”

“…An intense inflammatory process by pathogen infection may result in debris of cellular membranes of the bacteria and host cells, creating a substrate for calcium deposition (15). Indeed, several pathogens have been found in calcified tissues (10, 11). Also, a cross-reaction of antibodies to pathogen and human heat shock protein has been proposed as a link between pathogens and calcification (16).…”