Increased monocyte‐platelet aggregates and monocyte‐endothelial adhesion in healthy individuals with vitamin D deficiency
Hui Min Tay, Wei Hseun Yeap, Rinkoo Dalan, Siew Cheng Wong, Han Wei Hou
Abstract
Abstract Vitamin D deficiency is a major public health problem worldwide, linked to several chronic diseases including cardiovascular diseases. While immunomodulatory effects of vitamin D on monocytes have been reported in cardiovascular and metabolic diseases, there is limited understanding on monocyte phenotype in healthy individuals with suboptimal vitamin D levels and without any clinical diseases. In this work, we performed label‐free, microfluidic isolation of monocytes, and characterized their functional phenotype using flow cytometry and in vitro vascular models in healthy subjects with (n = 7) and without vitamin D deficiency (n = 16). Vitamin D deficient (VitD‐Def) subjects (25(OH)D 3 level < 26 ng/mL) expressed significant downregulation of vitamin D receptor (VDR) on monocytes as compared to controls ( P < .0001), and VDR expression was well‐associated with serum 25(OH)D 3 levels. Increased monocyte‐platelet aggregates (MPA), a marker for platelet activation, were also observed in VitD‐Def subjects ( P < .05) which suggests a pro‐inflammatory monocyte phenotype. Monocyte adhesion to endothelial cells, an early‐stage atherosclerosis event, was also higher in VitD‐Def individuals, and inversely correlated to serum 25(OH)D 3 level ( P < .05). Taken together, these results indicate the pro‐inflammatory state and atherogenic potential of monocytes in VitD‐Def healthy subjects, and propound the use of vitamin D supplementation as a prospective immunomodulatory and anti‐inflammatory therapy in atherosclerosis.