Abstract
BackgroundThis study aims to investigate the role of FPR 1/2/3 expressions in patients with obstructive sleep apnea (OSA).MethodWe made cross-sectional comparisons of FPR1/2/3 expressions of blood neutrophil, M1/M2a monocyte, and natural killer (NK) cell between 16 healthy subjects (HS), 16 primary snoring (PS) subjects, 46 treatment-naive OSA patients, and 18 severe OSA patients under long-term continuous positive airway pressure treatment (severe OSA on CPAP).ResultsFPR1 expressions on neutrophil were increased in treatment-naive OSA and severe OSA on CPAP groups versus either HS or PS. FPR2 expressions on neutrophil were decreased in treatment-naive OSA versus HS, and returned to normal in severe OSA on CPAP group. FPR1/FPR2 expression ratio on neutrophil was increased in treatment-naive OSA versus either HS or PS. Serum lipoxin A4, resolvin D1 levels, and FPR3 expressions of M1, M2a and NK cells were all decreased in treatment-naive OSA versus HS. OSA patients with hypertension had decreased FPR2 expressions on neutrophil and FPR3 expressions of NK cell. FPR1 expression, FPR1/FPR2 expression ratio on neutrophil, and FPR3 expression of M1 cell were all reversed after > 6-month CPAP treatment in 9 selected patients. In vitro intermittent hypoxia with re-oxygenation treatment in THP-1 cells resulted in increased FPR1/FPR2 expression ratio of M1 cells, and increased FPR1/FPR3 expression ratio of M2a cells.ConclusionsFPR1 over-expression and insufficiency of FPR2 and FPR3 in association with defective lipoxin A4 and resolving D1 production were associated with disease severity of OSA and its adverse consequences.
Highlights
Obstructive sleep apnea (OSA) is a clinical condition characterized by recurrent episodes of complete or partial obstruction of the upper airway, leading to sleep fragmentation and chronic intermittent hypoxia with re-oxygenation (IHR) during sleep
FPR1 expressions on neutrophil were increased in treatment-naive obstructive sleep apnea (OSA) and severe OSA on continuous positive airway pressure (CPAP) groups versus either healthy subjects (HS) or primary snoring (PS)
FPR1 over-expression and insufficiency of FPR2 and FPR3 in association with defective lipoxin A4 and resolving D1 production were associated with disease severity of OSA and its adverse consequences
Summary
Obstructive sleep apnea (OSA) is a clinical condition characterized by recurrent episodes of complete or partial obstruction of the upper airway, leading to sleep fragmentation and chronic intermittent hypoxia with re-oxygenation (IHR) during sleep. In parallel with ischemia-reperfusion injury, chronic IHR in OSA leads to sympathetic nervous system activation and oxidative stress with a resultant systemic inflammatory cascade and subsequent endothelial dysfunction, which may contribute to increased risk of cardiovascular disease, hypertension, stroke, and all-cause mortality[1, 2]. FPR1 is associated with pro-inflammatory responses, such as cytokine production, and superoxide production, while FPR2 is an unconventional receptor because it can convey contrasting biological signals, depending on the ligands[8, 9]. Serum amyloid protein A (SAA) and cathelicidin (LL-37) ligations result in FPR2/FPR1 heterodimerization, which leads to the induction of pro-inflammatory responses via JNK pathway signaling [10, 11]. This study aims to investigate the role of FPR 1/2/3 expressions in patients with obstructive sleep apnea (OSA)
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