CD36 expression intensity on different subpopulations of circulating monocytes depending on the extent of subclinical atherosclerosis

Abstract

It is known that chronic activation of innate immunity and persistent low-intensity inflammation play a crucial role in the initiation and progression of atherosclerosis. It was found that atherogenic lipoproteins can act as inducers of the inflammatory response through ligand-receptor interaction with pattern-recognizing receptors of immunocompetent cells, such as CD36 (SR-B2) and Toll-like receptors. It is suggested that expression of CD36 on circulating monocytes may represent the burden of systemic atherosclerosis and, therefore, act as its diagnostic marker. The aim of the present study was to assess the intensity of CD36 expression on circulating monocytes of different subpopulations in patients without established cardiovascular disease (CVD) depending on the extent of subclinical atherosclerosis of peripheral arteries. One hundred patients without established atherosclerotic CVD, 49 (49.0%) men and 51 (51.0%) women, were included in the study. Monoclonal antibody conjugates were used to phenotype monocyte subpopulations. The expression of CD36 on CD14++CD16- monocytes (classical monocytes), CD14+CD16+ monocytes (intermediate monocytes), CD14+CD16++ monocytes (non-classical monocytes) was determined by the average fluorescence intensity. There was a statistically significant decrease in CD36 expression intensity on classical and non-classical monocytes with increasing number of vascular basins affected by atherosclerosis. A statistically significant decrease in CD36 expression intensity on classical and non-classical monocytes was found in the patients with two vascular beds lesions in comparison with patients with a single vascular bed lesion upon pairwise comparisons.