Intensity of CD36 expression by monocyte subpopulations and blood lipid spectrum parameters in patients without established atherosclerotic cardiovascular disease

Abstract

Introduction. At the current stage of the study of atherosclerosis, it has been established that chronic activation of innate immunity, causing persistent low-intensity sterile inflammation, plays a crucial role at all stages of atherogenesis. Laboratory evaluation of signaling pathways associated with molecular patterns (DAMPs) in atherosclerosis and related to cardiovascular diseases (CVD) may contribute to the discovery of new diagnostic and prognostic markers. Objective: to study the relationship between lipid metabolism parameters and CD36 exposure to circulating monocytes in patientwithout established CVD. Material and methods . The study included 42 patients aged 40–64 years without established atherosclerotic CVD, 19 (45.2 %) men and 23 (54.7 %) women. Dyslipidemia was detected in 95.2 % of patients. The blood serum concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, glucose, glycated hemoglobin, high-sensitivity C-reactive protein (hs-CRP), creatinine were determined with subsequent calculation of glomerular filtration rate. Phenotyping of circulating monocyte subpopulations was performed by flow cytometry on a Navios 6/2 device (Beckman Coulter, USA). Results and discussion . According to the results of correlation analysis, non-HDL cholesterol levels were inversely correlated with absolute ( r = –0.394; p = 0.013) and relative ( r = –0.432; p = 0.006) content of CD14 + CD16 ++ CD36 + TLR2 + monocytes. LDL cholesterol levels were also inversely correlated with the relative content of CD14 + CD16 + CD36 + TLR2 + monocytes ( r = –0.417; p = 0.018). According to correlation analysis, the level of non-HDL cholesterol inversely correlated with the intensity of CD36 expression on classical ( r = –0.650; p < 0.0001), intermediate ( r = –0.323; p = 0.045) and non classical ( r = –0.480; p = 0.002) monocytes. Also, CD36 expression intensity on classical ( r = –0.449; p = 0.004) and non-classical ( r = –0.382; p = 0.016) monocytes was inversely correlated with remnant cholesterol levels. In addition, increased non-HLA cholesterol levels were associated with decreased TLR2 expression on CD14 + CD16 ++ monocytes ( r = –0.381; p = 0.018). It should be noted that a decrease in CD36 expression on intermediate monocytes was also associated with an increase in hs-CRP ( r = –0.657; p = 0.003). Conclusion . In patients without established atherosclerotic CVD, an increase in cholesterol content of atherogenic lipoprotein fractions was associated with a decrease in the number of CD14 + CD16 ++ and CD14 + CD16 + monocytes co-expressing CD36 and TLR2 as well as with a decrease in CD36 expression on classical, intermediate and non-classical monocytes.