THE ROLE OF CHLAMIDIA PNEUMONIA AND TNF-α IN DESTABILIZATION OF ATHEROSCLEROTIC PLAQUE BY HUMAN

Research objective: The aim of this work was a comparative study of the contents of the Chlamydia pneumoniae and TNF-α in the unstable and stable atherosclerotic lesions in humans and their role in the destabilization of atherosclerotic plaques. Material and methods: Investigated 50 aortic tissue samples received from 61 ± 7 years men who died from coronary heart disease. Verification of unstable progressive atherosclerotic plaques was conducted using histological staining Oil Red O and hematoxylin Mayer. Chlamydia pneumoniae identified in two ways: by using monoclonal antibodies and by modified Romanowski-Giemsa. Determination of TNF-α was made highly sensitive two-stage biotin-streptavidin method. Analysis of the results was carried out using a light microscope Leica DM 2500 and computer program «Leica Application Suite Version 3.4.0». Results: In unstable atherosclerotic lesions in the same areas and cell types that make up the inflammatory infiltrates, as well as in cells smooth muscle cells of these plaques are detected simultaneously Chlamydia pneumoniae and powerful inflammation cytokine TNF-α. In stable lesions intra- and extracellular expression of this cytokine is not detected. Conclusion: On the formation of unstable plaques a large impact could have the combined effect of Chlamydia pneumoniae and TNF-α, contributing to the development of the immunoinflamatory process in the vascular wall. Potential mechanism for strengthening action on the severity of the disease may be associated with direct or indirect influence of infection, as damage to the vascular wall, and increased production of proinflammatory cytokines cells, which are involved in the destabilization of plaque.