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Original Research: COPD |

Osteoprotegerin in Sputum Is a Potential Biomarker in COPDOsteoprotegerin in COPD

Masako To, MD; Kazuhiro Ito, PhD; Pilar M. Ausin, MD; Sergei A. Kharitonov, MD; Peter J. Barnes, DM, FCCP
Author and Funding Information

From the Airway Disease Section, National Heart and Lung Institute, Imperial College, London, England.

Correspondence to: Peter J. Barnes, DM, FCCP, Airway Disease Section, National Heart and Lung Institute, Imperial College, Dovehouse St, London, SW3 6LY, England; e-mail: p.j.barnes@imperial.ac.uk


Funding/Support: Financial support was provided by the National Heart and Lung Institute, Imperial College, London, England, and a Wellcome Trust Programme Grant.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(1):76-83. doi:10.1378/chest.10-1608
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Background:  COPD is characterized by chronic airflow limitation and inflammation of the respiratory tract. Several inflammatory biomarkers have been evaluated in COPD but are poorly related to disease severity and progression. Osteoprotegerin (OPG) is a glycoprotein mediator that is expressed in the lung and macrophages, so we have studied its concentration in induced sputum and macrophages of patients with COPD.

Methods:  OPG was measured by enzyme-linked immunosorbent assay in induced sputum of patients with COPD and control subjects.

Results:  OPG concentrations in induced sputum of patients with COPD (18.7 ± 18.6 ng/mL, n = 39) were significantly higher than those of healthy smokers (8.1 ± 5.6 ng/mL, n = 15), healthy nonsmokers (3.5 ± 3.8 ng/mL, n = 14), or patients with asthma (8.0 ± 5.4 ng/mL, n = 18). Sputum OPG levels in COPD negatively correlated with FEV1 and positively correlated with residual volume to total lung capacity ratio (RV/TLC) (r = 0.55, P < .05), transfer factor of the lung for carbon monoxide (r = −0.53, P < .05), and carbon monoxide transfer coefficient (r = −0.61, P < .01). By contrast, sputum IL-8 concentrations were related to disease severity but not to RV/TLC or gas diffusion. Airway macrophages and neutrophils were positive for OPG by immunocytochemistry in sputum and peripheral lung tissue. OPG induced matrix metalloproteinase-9 release from sputum macrophages in vitro.

Conclusions:  Sputum OPG may be a useful biomarker to monitor parenchymal destruction in COPD.

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