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Upregulation of pro-inflammatory cytokines in the intercostal muscles of COPD patients

¹ Muscle and Respiratory System Research Unit (URMAR), Respiratory Medicine Dept, Hospital del Mar, ² CEXS Dept, IMIM, and ³ Pompeu Fabra University, Barcelona, and ⁴ CIBER of Respiratory Diseases, ISCIII, Ministry of Health, Spain, ⁵ C. Casadevall and C. Coronell share the position of first author.

CORRESPONDENCE: J. Gea, Muscle and Respiratory System Research Unit (URMAR), IMIM, Hospital del Mar, c/ Doctor Aiguader 88, E-08003 Barcelona, Spain. Fax: 34 932213237. E-mail: jgea{at}imim.es

Keywords: Chronic lung disease, interleukin-1, interleukin-6, muscle function, respiratory muscle, tumour necrosis factor-

Received: December 26, 2005
Accepted June 22, 2007

Muscle dysfunction is a characteristic feature of chronic obstructive pulmonary disease (COPD). Recent studies suggest that cytokines may operate as local regulators of both muscle function and regeneration. The aim of the present study was to characterise the expression of different cytokines in the external intercostal muscle of COPD.

Muscle biopsies were obtained from 25 stable COPD patients and eight healthy controls. Local tumour necrosis factor (TNF)-, interleukin (IL)-1ß, -6 and -10 expressions (real-time PCR and ELISA), sarcolemmal damage (immunohistochemistry), and the transcript levels of CD18 were assessed.

Muscle TNF- and IL-6 transcripts were significantly higher in COPD patients compared with controls, and IL-1ß and sarcolemmal damage showed a strong tendency in the same direction. Similar results were observed at protein level. The CD18 panleukocyte marker was similar in COPD and controls. Respiratory muscle function was impaired in COPD patients and it correlated to both the severity of lung function impairment and TNF- muscle expression.

Chronic obstructive pulmonary disease is associated with the upregulation of pro-inflammatory cytokines in the intercostal muscles. This phenomenon might be involved in respiratory muscle dysfunction.

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