Potential inflammatory markers in obstructive sleep apnea-hypopnea syndrome.

Dongmei Lu,Ling Zhou,Nanfang Li,Xiaoguang Yao

doi:10.17305/bjbms.2016.1579

Abstract

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a complex chronic inflammatory respiratory disease with multiple pathogenic factors and high morbidity and mortality. Serum levels of nuclear factor-κB (NF-κB), hypoxia-inducible factor-1 alpha (HIF-1α), and surfactant protein D (SPD) were investigated in OSAHS patients, to determine their clinical significance and correlation with the pathogenesis. Patients were classified into a mild and moderate OSAHS group (n = 25) and severe OSAHS group (n = 33). Twenty healthy patients served as a control group. Peripheral blood levels of NF-κB, HIF-1α, and SPD were determined by Western blot, and a correlation analysis was performed. Severe OSAHS patients received nasal continuous positive airway pressure (nCPAP) therapy and were followed up after 2 months. NF-κB p65, HIF-1α, and SPD expression levels were determined after valid nCPAP therapy. NF-κB p65 and HIF-1α expression was significantly higher in severe OSAHS group than in the other two groups (p < 0.01), and was positively correlated with the apnea-hypopnea index (AHI) (r = 0.696, p < 0.001; r = 0.634, p < 0.001). SPD expression was significantly lower in severe OSAHS group than in the control group (p < 0.01) and mild and moderate OSAHS group (p < 0.01), and was negatively correlated with AHI (r = -0.569, p < 0.001). OSAHS pathogenesis was associated with changes in NF-κB, HIF-1α, and SPD protein expression levels. nCPAP therapy could improve the clinical characteristics of the patients, lower serum NF-κB and HIF-1α levels, and increase serum SPD levels. We conclude that OSAHS is related to the expression of NF-κB, HIF-1, and SPD.

Highlights

Obstructive sleep apnea-hypopnea syndrome (OSAHS), which is characterized by repetitive episodes of airflow reduction or cessation due to upper airway collapse during sleep, often causes chronic intermittent hypoxia, repetitive waking, and sleep fragmentation
The serum surfactant protein D (SPD) levels decreased with OSAHS severity; the lowest level was observed in severe OSAHS group (Table 1)
In severe OSAHS group, both nuclear factor-κB (NF-κB) p65 (r = 0.513, 0.002) and HIF-1α (r = 0.343, p = 0.003) expression levels were negatively correlated with SPD expression (Table 1)

Summary

Introduction

Obstructive sleep apnea-hypopnea syndrome (OSAHS), which is characterized by repetitive episodes of airflow reduction (hypopnea) or cessation (apnea) due to upper airway collapse during sleep, often causes chronic intermittent hypoxia, repetitive waking, and sleep fragmentation. OSAHS increases all-cause mortality and the risk of death, and it results in multi-system and multi-organ damage [1,2]. As an independent risk factor for hypertension, coronary disease, left heart failure, pulmonary heart disease, myocardial infarction, and stroke, OSAHS is closely related to cardiac and cerebrovascular diseases. The prevalence of OSAHS has risen from 3 to 10% in adult population [3,4]. OSAHS is considered a complex, multi-factor and multigene disease, and its pathogenesis remains unexplored.

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