PMID- 19652426
OWN - NLM
STAT- MEDLINE
DCOM- 20091104
LR  - 20220408
IS  - 1349-7235 (Electronic)
IS  - 0918-2918 (Linking)
VI  - 48
IP  - 15
DP  - 2009
TI  - Production of inflammatory mediators by monocytes in patients with obstructive 
      sleep apnea syndrome.
PG  - 1255-62
AB  - 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)-alpha, 
      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-alpha, MCP-1, and MMP-9 in 
      the culture supernatants were determined by ELISA. RESULTS: In severe patients, 
      the TNF-alpha production by monocytes was significantly elevated as compared to 
      that before sleep (p<0.01). In all OSAS patients, the TNF-alpha production after 
      sleep was significantly correlated with AHI (p<0.01), ODI (p<0.01) and % time in 
      SpO(2)<90% (p<0.05), and inversely correlated with the lowest SpO(2) (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.
FAU - Tamaki, Shinji
AU  - Tamaki S
AD  - Second Department of Internal Medicine, Nara Medical University, Nara.
FAU - Yamauchi, Motoo
AU  - Yamauchi M
FAU - Fukuoka, Atsuhiko
AU  - Fukuoka A
FAU - Makinodan, Kiyoshi
AU  - Makinodan K
FAU - Koyama, Noriko
AU  - Koyama N
FAU - Tomoda, Koichi
AU  - Tomoda K
FAU - Yoshikawa, Masanori
AU  - Yoshikawa M
FAU - Kimura, Hiroshi
AU  - Kimura H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090803
PL  - Japan
TA  - Intern Med
JT  - Internal medicine (Tokyo, Japan)
JID - 9204241
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Adult
MH  - Body Mass Index
MH  - Case-Control Studies
MH  - Chemokine CCL2/biosynthesis
MH  - Continuous Positive Airway Pressure
MH  - Female
MH  - Humans
MH  - Hypoxia/metabolism
MH  - In Vitro Techniques
MH  - Inflammation Mediators/*metabolism
MH  - Male
MH  - Matrix Metalloproteinase 9/biosynthesis
MH  - Middle Aged
MH  - Monocytes/*metabolism
MH  - Sleep Apnea, Obstructive/*metabolism/pathology/therapy
MH  - Stress, Physiological
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/biosynthesis
EDAT- 2009/08/05 09:00
MHDA- 2009/11/05 06:00
CRDT- 2009/08/05 09:00
PHST- 2009/08/05 09:00 [entrez]
PHST- 2009/08/05 09:00 [pubmed]
PHST- 2009/11/05 06:00 [medline]
AID - JST.JSTAGE/internalmedicine/48.2366 [pii]
AID - 10.2169/internalmedicine.48.2366 [doi]
PST - ppublish
SO  - Intern Med. 2009;48(15):1255-62. doi: 10.2169/internalmedicine.48.2366. Epub 2009 
      Aug 3.