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[Is arteriosclerosis an infectious disease?].

There are three findings suggesting the inflammatory and immunogenic nature of the atherosclerosis: Firstly the colocalisation of macrophages/monocytes and T-lymphocytes in all phases of the atherosclerosis, starting with intimal damages and developing into the end stage of atheromatous plaques, secondly the production of cytokines and thirdly the expression of MHC II antigens. The persisting chlamydia pneumoniae bacteria infection, which has been repeatedly detected in the intima, sustains this inflammatory process. Endothelial dysfunction and an expression of adhesion molecules, which might have been triggered by the chlamydial infection, could lead to atherosclerotic lesions according to the "response to injury" theory. The chlamydiae specific findings can well be integrated into this concept: Two of three classical Koch postulates are nearly fulfilled. There is additional direct and indirect evidence--particularly the first positive results of oral antibiotic therapy after acute myocardial infarction--suggesting a causative role. The unfavourable changes in the lipid profile, which might be brought about by the infection, may also contribute. Repeated chlamydial reinfections trigger the immune system through the cellular memory of T-lymphocytes sustaining the intramural inflammatory process. This leads to an activation of metalloproteinases with a fissuring on the plaques and finally to thrombosis. If this suggested link is confirmed, the latent chlamydia infections could be another treatable risk factor apart from the classical cardiovascular risk factors.