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Skeletal muscle inflammation and nitric oxide in patients with COPD.

Authors :
Montes de Oca M
Torres SH
De Sanctis J
Mata A
Hernández N
Tálamo C
Source :
The European respiratory journal [Eur Respir J] 2005 Sep; Vol. 26 (3), pp. 390-7.
Publication Year :
2005

Abstract

In chronic obstructive pulmonary disease (COPD) the presence of systemic inflammation has been associated with peripheral muscle abnormalities and weight loss. To study whether inflammatory factors are important in these processes, the present study compared the skeletal muscle levels of nitrite, nitrate, nitrotyrosine, neuronal, endothelial and inducible nitric oxide synthases (nNOS, eNOS, and iNOS, respectively), and inflammatory markers (tumour necrosis factor (TNF)-alpha, CD154 and CD163) in 15 patients (forced expiratory volume in one second 43+/-11%) and 14 controls. All these markers were also compared between patients with normal and low body weight. Nitrite (12.5+/-2.6 versus 17.0+/-3.4 micromol.mg(-1) protein), nitrate (20.7+/-2.4 versus 24.4+/-4.5 micromol.mg(-1) protein) and eNOS (31.9+/-4.6 versus 43.6+/-7.5 ng.mg(-1) protein) were lower in COPD patients than in controls. Nitrotyrosine (25.6+/-5.4 versus 6.6+/-3.3 ng.mg(-1) protein), iNOS expression (32+/-9.5 versus 7.16+/-2.7 ng.mg(-1) protein), TNF-alpha (257+/-160 versus 48.3+/-4.4 pg.mg(-1) protein) and CD163 (6.4+/-2.1 versus 0.8+/-0.4 ng.mg(-1) protein) were higher in COPD patients than in controls. CD154 levels were 15.7+/-7.0 ng.mg(-1) protein in COPD patients and undetectable in controls. Similar levels of all these markers were observed in COPD patients with normal and low body weight. In conclusion, these findings suggest the presence of an inflammatory process in the muscle tissue of chronic obstructive pulmonary disease patients, and argue in favour of its participation in the pathogenesis of skeletal muscle abnormalities.

Details

Language :
English
ISSN :
0903-1936
Volume :
26
Issue :
3
Database :
MEDLINE
Journal :
The European respiratory journal
Publication Type :
Academic Journal
Accession number :
16135718
Full Text :
https://doi.org/10.1183/09031936.05.00107404