Abstract

Patients with obstructive sleep apnea (OSA) experience partial or complete upper airway collapses during sleep resulting in nocturnal hypoxia-normoxia cycling, and continuous positive airway pressure (CPAP) is the golden treatment for OSA. Nevertheless, the exact mechanisms of action, especially the transcriptome effect of CPAP on OSA patients, remain elusive. The goal of this study was to evaluate the longitudinal alterations in peripheral blood mononuclear cells transcriptome profiles of OSA patients in order to identify the hub gene and immune response. GSE133601 was downloaded from Gene Expression Omnibus (GEO). We identified black module via weighted gene co-expression network analysis (WGCNA), the genes in which were correlated significantly with the clinical trait of CPAP treatment. Finally, eleven hub genes (TRAV10, SNORA36A, RPL10, OBP2B, IGLV1-40, H2BC8, ESAM, DNASE1L3, CD22, ANK3, ACP3) were traced and used to construct a random forest model to predict therapeutic efficacy of CPAP in OSA with a good performance with AUC of 0.92. We further studied the immune cells infiltration in OSA patients with CIBERSORT, and monocytes were found to be related with the remission of OSA and partially correlated with the hub genes identified. In conclusion, these key genes and immune infiltration may be of great importance in the remission of OSA and related research of these genes may provide a new therapeutic target for OSA in the future.

Highlights

  • obstructive sleep apnea (OSA) is a highly prevalent sleep disorder, characterized by repetitive partial or complete airway collapse resulting in apneic events during sleep, sleep fragmentation and chronic intermittent hypoxia

  • A total of 15 samples with post continuous positive airway pressure (CPAP) therapy and 15 corresponding paired control samples of pre-treatment were included into the analysis

  • The results showed that monocytes had the highest proportion and the number of monocytes in post-CPAP group was higher than control group (P

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Summary

Introduction

OSA is a highly prevalent sleep disorder, characterized by repetitive partial or complete airway collapse resulting in apneic events during sleep, sleep fragmentation and chronic intermittent hypoxia. The direct consequence of the intermittent hypoxia is an oxidative imbalance, with reactive oxygen species production, inflammatory cytokines (IL2, IL4, IL6), lipid peroxidation and cell-free DNA production [1], and patients with OSA have higher risk of developing metabolic comorbidities and cardiovascular disorders [2,3,4]. Identification of key genes and immune infiltration modulated by CPAP in obstructive sleep apnea

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