The activation of the inflammatory cytokines in overweight patients with mild obstructive sleep apnoea.
It is widely accepted that obstructive sleep apnoea (OSA) is linked with cardiovascular diseases. The relationship is complex and remains still poorly understood. The presence of chronic systemic inflammation has been connected with pathogenesis of both OSA and cardiovascular diseases. While atherogenesis is believed to be a process of many years, little is known about the potential impact of the largest OSA subgroup, mild OSA, on the development of cardiovascular diseases. The aim of the present study was to assess whether untreated mild OSA is associated with an activation of inflammatory cytokine system. The adult study population consisted of two groups: 84 patients with mild OSA [apnoea-hypopnoea index (AHI) 5-15 h(-1)] and 40 controls (AHI <5 h(-1)). Serum concentrations of pro- and anti-inflammatory cytokines were measured before any interventions. After adjustments for age, sex, body mass index, fat percentage, most important cardiometabolic and inflammatory diseases, and non-steroidal anti-inflammatory medication, the mean level of tumour necrosis factor-alpha was significantly elevated (1.54 versus 1.17 pg mL(-1), P = 0.004), whereas the level of interleukin-1 beta (IL-1 beta) was reduced (0.19 versus 0.23 pg mL(-1), P = 0.004) in patients with mild OSA compared with controls. The concentrations of the protective anti-inflammatory cytokines, interleukin-10 (1.28 versus 0.70 pg mL(-1), P < 0.001) and interleukin-1 receptor antagonist (478 versus 330 pg mL(-1), P = 0.003) were elevated in the OSA group. The concentrations of C-reactive protein increased, but IL-1 beta decreased along with the increase of AHI. Mild OSA was found to be associated not only with the activation of the pro-inflammatory, but also with the anti-inflammatory systems.
Sahlman
Johanna
J
Department of Otorhinolaryngology, Institute of Clinical Medicine, Kuopio University Hospital and University of Kuopio, Kuopio, Finland.
Miettinen
Kati
K
Peuhkurinen
Keijo
K
Seppä
Juha
J
Peltonen
Markku
M
Herder
Christian
C
Punnonen
Kari
K
Vanninen
Esko
E
Gylling
Helena
H
Partinen
Markku
M
Uusitupa
Matti
M
Tuomilehto
Henri
H
D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis / Q000502:physiology; D002318:Cardiovascular Diseases / Q000097:blood / Q000503:physiopathology; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood* / Q000502:physiology; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood / Q000502:physiology; D016753:Interleukin-10 / Q000097:blood / Q000502:physiology; D053583:Interleukin-1beta / Q000097:blood / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000276:immunology; D010100:Oxygen / Q000097:blood; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000502:physiology
D015415:Biomarkers; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002097:C-Reactive Protein; D010100:Oxygen