Atherosclerosis, inflammation, and infection

In recent years, it has been shown that inflammation plays an important rol e in the pathogenesis of atherosclerosis. Activated macrophages, T lymphocy tes, and mast cells are present in atherosclerotic plaques, which has led t o the notion that the inflammatory response is an immune-mediated process. Complicated lesions, moreover, appear to be associated with an increase in the amount of the inflammatory response and in these patients, increased le vels of acute phase proteins are present. The appreciation that atheroscler osis is an immune-mediated inflammatory disease has also led to renewed int erest in the potential role of infectious agents in initiating or modulatin g atherosclerosis. Seroepidemiological studies have shown raised antibody t itres against several micro-organisms. However, as yet, there are hardly an y data available that provide a sound scientific basis for an infectious or igin. Of all potential candidate organisms, Chlamydia pneumoniae appears as the one most likely involved in atherogenesis. C. pneumoniae has been retr ieved from atherosclerotic tissues; the level of raised plasma titres corre lates with the severity of symptomatic atherosclerotic: disease; and the in cidence of C. pneumoniae-responsive T cells in peripheral blood is increase d in patients with coronary heart disease. It also appears that in some pat ients T cells generated from atherosclerotic plaques respond to C. pneumoni ae. At the present state of knowledge, however, it is fair to state that th e relationship between infection, intraplaque inflammation, and atheroscler osis still remains hypothetical, despite the increasing evidence that such a relationship could exist. Copyright (C) 2000 John Wiley & Sons, Ltd.