Chlamydia pneumoniae and multiple infections in the aorta contribute to atherosclerosis.

Our previous study on herpesvirus infection including Herpes simplex virus type 1 (HSV-1), Epstein-Barr virus (EBV), cytomegalovirus (CMV) and atherosclerosis revealed that the prevalence of herpesvirus is higher in atherosclerotic aorta than in non-atherosclerotic aorta. Infections with two or three forms of the virus have been found only in atherosclerotic aorta. In our current study, we examined both Chlamydia pneumoniae and Chlamydia trachomatis in herpesvirus-infected aortic tissues, by means of immunohistochemistry, polymerase chain reaction, Southern hybridization, in situ hybridization, electron microscopy and electron-microscopic immunohistochemistry. In particular, the bacteria were found in atherosclerotic lesions. In atherosclerotic aorta, 40% of tissues examined were positive for C. pneumoniae in contrast to absence of this bacteria in non-atherosclerotic aorta. Elementary bodies of C. pneumoniae were found in macrophage-like cells in the intima of atherosclerotic aorta by electron microscopy. Chlamydia trachomatis was not found in both atherosclerotic and non-atherosclerotic aorta. Our findings suggest that multiple infections in aortic tissue contribute to the development of atherosclerosis. Furthermore, the absence of C. pneumoniae compared to herpesviruses in normal arterial tissue suggests that C. pneumoniae is specific for atherosclerotic lesions. In contrast to 'abortive infection' of viruses in arteries, C. pneumoniae infection was demonstrated in macrophages by electron microscopy and electron-microscopic immunohistochemistry in atherosclerotic lesion. Chlamydia pneumoniae may be the most important pathogen related to the development of atherosclerosis.