Blood Monocyte Phenotypes and Effect of Selenium on Mononuclear Cells in Coronary Artery Disease : A Special Focus on Monocyte Migration Markers and STAT-3/IL-6 Axis

Abstract

Chronic inflammation is a key factor in the development of atherosclerosis, the underlying pathological mechanism of coronary artery disease (CAD), where circulating blood monocytes play a crucial role. These monocytes are classified into three subtypes: classical, intermediate and non-classical. Further, pro-inflammatory cytokines secreted by the mononuclear cells are pivotal in sustaining the state of inflammation in CAD. Hence, the main aim of the study was (i) to investigate the existing state of inflammation among CAD patients in terms of (a) monocytes subtypes and (b) pro-inflammatory cytokines and (ii) to intervene the inflamed state with a therapeutic concentration of selenium, in-vitro. The study found that CAD patients exhibited ongoing inflammation, characterized by (i) alterations in monocyte subtypes, including a decrease in classical monocytes and an increase in non-classical monocytes, (ii) heightened CCR1 expression in classical monocytes, suggesting potential differentiation towards inflamed monocytes or macrophages, and (iii) elevated IL-6 cytokine levels. Selenium in-vitro treatment diminished the conversion of classical monocytes into the intermediate and non-classical subsets. Moreover, selenium in-vitro intervention was found to minimize inflammation by hampering the STAT-3 activity and thereby lowering the production of pro-inflammatory cytokines, including IL-6 and TNF-α, by CAD mononuclear cells. In conclusion, the study highlights the potential of selenium to modulate the inflammatory processes and might hold promising potential as a therapeutic approach for CAD patients.