• Yang Xiang, Bin Liang, Xiaokang Zhang, and Fang Zheng.
• Center for Gene Diagnosis, and Clinical Lab, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan 430071, China.
• Int J Med Sci. 2020 Jan 1; 17 (14): 2171-2179.

AbstractBackground: Increased expressions of CD16 on classical monocytes precede their transition to intermediate monocytes. Thus far, the influence of lipids on the expression of CD14 and CD16 on monocyte subsets in coronary atherosclerosis (CA) remains unclear. The aim of this study was to investigate the underlying association between blood lipids and the expression of CD14 and CD16 on monocyte subsets. Methods: This study enrolled 112 healthy controls and 110 CA patients. Monocyte subsets [CD14++CD16- (classical), CD14++CD16+ (intermediate) and CD14+CD16++ (non-classical)] were analyzed by flow cytometry. Median fluorescent intensity (MFI) was used to evaluate the expression levels of CD14 and CD16 on monocyte subsets. Results: Compared with the control group, the expression of CD16 was significantly increased on all three monocyte subsets in the patient group. Correlation analysis revealed that serum HDL-C was inversely associated with the expression of CD16 on intermediate monocytes after Bonferroni correction in the control group. In addition, a significant decrease in classical monocytes and an increase in intermediate monocytes were detected in patients. In linear regression analysis, intermediate monocytes showed an inverse association with serum HDL-C in the control group. Although CD14 was correlated with serum TC and HDL-C, there was no statistical difference in CD14 expression between the two groups. Conclusion: Low serum HDL-C may induce upregulation of CD16 on classical monocytes, which may in turn lead to the increase of intermediate monocytes in coronary atherosclerosis patients.© The author(s).

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