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Adipokines NUCB2/Nesfatin-1 and Visfatin as Novel Inflammatory Factors in Chronic Obstructive Pulmonary Disease

COPD (chronic obstructive pulmonary disease) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, adipose tissue mediated inflammation has gathered increasing interest in the pathogenesis of the disease. In this study, we investigated the role of novel ad...

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Published in:Mediators of Inflammation 2014-01, Vol.2014 (2), p.116-121
Main Authors: Leivo-Korpela, Sirpa, Lehtimäki, Lauri, Hämälainen, Mari, Vuolteenaho, Katriina, Kööbi, Lea, Järvenpää, Ritva, Kankaanranta, Hannu, Saarelainen, Seppo, Moilanen, Eeva
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Language:English
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Summary:COPD (chronic obstructive pulmonary disease) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, adipose tissue mediated inflammation has gathered increasing interest in the pathogenesis of the disease. In this study, we investigated the role of novel adipocytokines nesfatin-1 and visfatin in COPD by measuring if they are associated with the inflammatory activity, lung function, or symptoms. Plasma levels of NUCB2/nesfatin-1 and visfatin were measured together with IL-6, IL-8, TNF-α, and MMP-9, lung function, exhaled nitric oxide, and symptoms in 43 male patients with emphysematous COPD. The measurements were repeated in a subgroup of the patients after four weeks’ treatment with inhaled fluticasone. Both visfatin and NUCB2/nesfatin-1 correlated positively with plasma levels of IL-6 (r=0.341, P=0.027 and rho=0.401, P=0.008, resp.) and TNF-α (r=0.305, P=0.052 and rho=0.329, P=0.033, resp.) and NUCB2/nesfatin-1 also with IL-8 (rho=0.321, P=0.036) in patients with COPD. Further, the plasma levels of visfatin correlated negatively with pulmonary diffusing capacity (r=-0.369, P=0.016). Neither of the adipokines was affected by fluticasone treatment and they were not related to steroid-responsiveness. The present results introduce adipocytokines NUCB2/nesfatin-1 and visfatin as novel factors associated with systemic inflammation in COPD and suggest that visfatin may mediate impaired pulmonary diffusing capacity.
ISSN:0962-9351
1466-1861
DOI:10.1155/2014/232167