Internal Medicine
Online ISSN : 1349-7235
Print ISSN : 0918-2918
ISSN-L : 0918-2918
ORIGINAL ARTICLES
Production of Inflammatory Mediators by Monocytes in Patients with Obstructive Sleep Apnea Syndrome
Shinji TamakiMotoo YamauchiAtsuhiko FukuokaKiyoshi MakinodanNoriko KoyamaKoichi TomodaMasanori YoshikawaHiroshi Kimura
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JOURNAL OPEN ACCESS

2009 Volume 48 Issue 15 Pages 1255-1262

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Abstract

Background Obstructive sleep apnea syndrome (OSAS) is known to be a risk factor of cardiovascular events. However, the precise mechanism linking the two has not been fully elucidated.
Objective The aim of this study was to investigate the effect of hypoxic stress on the production of tumor necrosis factor (TNF)-α, monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-9 (MMP-9) by monocytes.
Methods Thirty-three OSAS patients and 13 healthy control subjects were enrolled. The OSAS patients were classified as mild-to-moderate (13) and severe (20). Venous blood samples were collected before and after sleep as well as after long-term nasal continuous positive airway pressure (CPAP) treatment for the purpose of isolation of monocytes. Peripheral blood monocytes were isolated using standard methods. Monocytes were cultured under lipopolysaccharide stimulation for 24 hours, and TNF-α, MCP-1, and MMP-9 in the culture supernatants were determined by ELISA.
Results In severe patients, the TNF-α production by monocytes was significantly elevated as compared to that before sleep (p<0.01). In all OSAS patients, the TNF-α production after sleep was significantly correlated with AHI (p<0.01), ODI (p<0.01) and % time in SpO2<90% (p<0.05), and inversely correlated with the lowest SpO2 (p<0.01). The production of MCP-1 and MMP-9 by monocytes was significantly elevated compared to that before sleep in severe patients (p<0.05). The production of these mediators by monocytes was significantly decreased after long-term nasal CPAP treatment (p<0.05).
Conclusion These results indicate that OSAS-induced hypoxic stress activates the production of inflammatory mediators by monocytes.

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© 2009 by The Japanese Society of Internal Medicine
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