Activated CD8+ T-lymphocytes in obstructive sleep apnoea

Abstract

T-lymphocytes are implicated in the development of atherosclerosis. The aim of this study was to assess whether the CD8+ T-lymphocytes of obstructive sleep apnoea (OSA) patients undergo phenotypic and functional changes that may exaggerate atherogenic sequelae in OSA.A total of 36 OSA patients, 17 controls and 15 single-night-treated OSA patients were studied. Phenotype and cytotoxicity against K562 target cells were analysed by flow cytometry. Cytotoxicity against human umbilical vein endothelial cells (HUVECs) was assessed by 51 Cr release assay.The cytotoxicity of the CD8+ T-lymphocytes of OSA patients against K562 and HUVECs was significantly greater than controls. This increased cytotoxicity directly depended on the presence of perforin and natural killer receptors (CD56, CD16), which were significantly increased in OSA CD8+ T-lymphocytes. Also the percentage of the CD56bright subset, which mediates initial interactions with vascular endothelium, significantly increased in OSA. Nasal continuous positive airway pressure treatment significantly decreased CD8+ T-cell cytotoxicity and CD56 expression, and was positively correlated with natural killer inhibitory NKB1 receptor expression either after a single-night treatment or after a prolonged treatment.In conclusion, the CD8+ T-lymphocytes of obstructive sleep apnoea patients undergo phenotypic and functional changes, rendering them cytotoxic to target cells via increased CD56+/perforin+ expression, which can be ameliorated by nasal continuous positive airway pressure treatment. These results are compatible with the current authors' hypothesis of atherogenic sequelae in obstructive sleep apnoea.

Sleep Apnea and Metabolic Dysfunction: Cause or Co-Relation?

“…Compared to normal subjects, sleep apnea patients have higher levels of circulating adhesion molecules (123)(124)(125)(126)(127)(128)(129) and inflammatory cytokines including IL-6 and TNF-α which decrease with effective CPAP therapy (34;112;130-135). In addition, studies examining specific leukocyte populations reveal that patients with sleep apnea also exhibit monocyte and lymphocyte activation which improves with CPAP therapy (136)(137)(138)(139). While the mechanisms through which sleep apnea disrupts normal immune function are poorly understood, intermittent hypoxemia is likely to play a leading role.…”

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

“…Several studies have demonstrated upregulation of leukocyte adhesion molecule expression in OSAS [29,[35][36][37][38][39]. This increased expression of adhesion molecules is associated with increased avidity toward endothelial cells and a subsequent enhancement in inflammationmediated endothelial dysfunction.…”

The influence of patent foramen ovale on oxygen desaturation in obstructive sleep apnoea

“…KEYWORDS: Echocardiography, heart septal defects, hypoxia, obstructive sleep apnoea, patent foramen ovale O bstructive sleep apnoea (OSA) is a common disorder that affects 5-15% of the middle-aged population and has been identified as a risk factor for cardiovascular disease [1][2][3]. Patent foramen ovale (PFO) is also a common condition, present in 25% of the adult population, which constitutes a risk factor for cryptogenic stroke as well as a potential contributor to hypoxaemia in patients, both with and without pulmonary disease [4][5][6][7].…”