[Effect of Chlamydia pneumoniae infection on carotid atherosclerosis development]

Recently, a growing number of epidemiological, histopathological and microbiological studies have shown that chronic Chlamydia pneumoniae (C. pneumoniae) infection accelerates the progression of atherosclerosis of carotid and cerebral arteries and thus could constitute a risk factor for stroke. We present a number of mechanisms postulated in recent papers that link C. pneumoniae infection with the development of atherosclerosis. The one most important seems to be the effect of activation of nuclear factor--kappa B and the phenomenon of antigenic mimicry between human and C. pneumoniae heat shock proteins. We also discuss the problem of immunological reaction against myosin filaments of carotid artery wall smooth muscle cells and the problem of antigenic mimicry between heavy chains of myosin filaments and antigens presented on C. pneumoniae outer membrane.