Infection with Chlamydia pneumoniae and atherosclerosis: a review.

There are numerous studies that were able to find C. pneumoniae infections as a contributing factor in atherosclerosis pathogenesis. Positive serology for C. pneumoniae was found in most studies in patients with atherosclerosis (IgG, IgA, IgM). Most studies were able to correlate an elevated IgA antibody titer rather than the IgG titer to the risk for atherosclerosis. C. pneumoniae and its components (DNA, antigens) were detected in atherosclerotic plaques using immunohistochemistry, PCR, electron microscopy and cell cultures. C. pneumoniae has been located in endothelium, smooth muscle cells and macrophages of arterial wall with atherosclerosis but not in normal arteries. Cellular models have shown that C. pneumoniae is able to replicate in endothelium, macrophages and smooth muscle cells. A high C. pneumoniae antibody titer was found to correlate with high level of LDL and triglycerides and low level of HDL. C. pneumoniae infection increases platelet adhesion and adhesion molecules at the surface of endothelium. C. pneumoniae could be a cofactor for atherosclerosis combined with high level of lipids as shown in an animal model but not alone. Strong cellular and humoral immunity have been found in men with atherosclerosis and positive C. pneumoniae titers. This organism could be found in diverse arteries with atherosclerosis. One particular C. pneumoniae strain (AR 39) appears to be more frequently involved in atherosclerosis. Antibiotic treatment with azithromycin appears to be protective against atherosclerosis complications. However, there is as yet no conclusive evidence that C. pneumoniae causes atherosclerosis, but most likely it may enhance this process. Two large randomized clinical trials are currently underway evaluating azithromycin treatment in patients with atherosclerosis which will hopefully give us answers about the role of antibiotic treatment.