Increased Adhesion Molecules Expression and Production of Reactive Oxygen Species in Leukocytes of Sleep Apnea Patients

TLDR

Obstructive sleep apnea is linked to higher cardiovascular morbidity and mortality, partly because free radicals and adhesion molecules contribute to atherosclerosis. The study examined whether expression of CD15, CD11c, CD11b, and CD64 on leukocytes correlates with reactive oxygen species production in OSA patients compared to controls. Researchers exposed monocytes to hypoxia in vitro, assessed their adhesion to cultured endothelial cells, and evaluated changes after nasal continuous positive airway pressure treatment. OSA patients showed higher CD15 and CD11c expression, greater monocyte adhesion, and elevated ROS in certain leukocyte subsets, while hypoxia induced CD15 upregulation in control monocytes; nCPAP reduced CD15/CD11c expression, basal ROS in CD11c⁺ monocytes, and monocyte adhesion, supporting a role for these factors in sleep apnea–related cardiovascular risk.

Abstract

Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Free radicals and adhesion molecules were implicated in the pathogenesis of atherosclerosis leading to cardiovascular disorders. Therefore, we investigated the link between CD15, CD11c, CD11b, and CD64 expression on leukocytes and their ability to generate reactive oxygen species (ROS) in patients with OSA and control volunteers. We also studied the effects of hypoxia in vitro on monocytes from control subjects and the ability of monocytes from both groups to adhere to human endothelial cells in culture. The effect of nasal continuous positive airway pressure (nCPAP) treatment was studied as well. We found that OSA was associated with increased expression of adhesion molecules CD15 and CD11c on monocytes, increased adherence of monocytes in culture to human endothelial cells, increased intracellular ROS production in some monocyte and granulocyte subpopulations, and upregulation of CD15 expression due to hypoxia in vitro in monocytes of control subjects. Furthermore, nCPAP treatment was associated with downregulation of CD15 and CD11c monocyte expression and decreased basal ROS production in CD11c+ monocytes. Monocyte adherence to endothelial cells decreased as well. Our findings provide one of the possible mechanisms for explaining the high rate of cardiovascular morbidity in patients with sleep apnea.