Abstract

Obstructive sleep apnea (OSA) is characterized by nocturnal breathing intermissions resulting in oxidative stress and eventually, a low-grade systemic inflammation. The study aimed to investigate the impact of positive airway pressure (PAP) therapy on the inflammatory milieu as measured by monocyte and T cell phenotypic alterations. Participants were assessed for their OSA severity before PAP therapy and about six months later, including patient-reported outcome and therapy usage by telemetry readout. The distributions of the CD14/CD16-characterized monocyte subsets as well as the CD4/CD8-characterized effector T cell subsets with regard to their PD-1 and PD-L1 expression were analyzed by flow cytometry from blood samples. Data of 25 patients revealed a significant reconstitution of the monocyte subset distribution and a decrease in PD-L1 expression on pan-monocytes and CD8+ T cells without an association to initial AHI and overweight. The PD-1 expression was still increased on T cell subsets, especially on CD4+ TH17/22 cells. We conclude that PAP therapy might have a rapid effect on the monocyte phenotype and overall PD-L1 expression levels. However, T cell immune alterations especially on TH17/22 cells persist longer, indicating an ongoing disturbance of the adaptive immune system.

Highlights

  • Obstructive sleep apnea (OSA) represents a substantial and frequent disease of recurrent breathing intermissions, resulting in a partial or complete cessation of the airflow in the upper airways followed by reoxygenation [1]

  • The present study was undertaken to investigate the impact of positive airway pressure (PAP) therapy on percentages of monocyte subsets and T cell immune alterations, distinguishing between

  • The expression levels of PD-1 and PD-L1 on the peripheral T cells of OSA patients were analyzed for CD3+ CD4+ and the CD3+ CD8+ subsets and monocytes using flow cytometry

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Summary

Introduction

Obstructive sleep apnea (OSA) represents a substantial and frequent disease of recurrent breathing intermissions, resulting in a partial (hypopnea) or complete cessation (apnea) of the airflow in the upper airways followed by reoxygenation [1]. The disease leads to intermitted hypoxia and nocturnal oxidative stress, which trigger a low-grade systemic inflammation. This condition promotes an activation of different immune cells such as lymphocytes and monocytes that secrete high amounts of inflammatory cytokines and adhesion molecules [2,3]. It has been shown to improve daytime sleepiness, quality of life, and depressive symptoms, as well as reduce risk for cardiovascular disease and mortality [5,6,7,8], whereas the impact on the last mentioned is highly debated [9]

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