Department of Respiratory Medicine, Tampere University Hospital, PL 2000, 33521 Tampere, Finland ; The Immunopharmacology Research Group, School of Medicine, University of Tampere and Tampere University Hospital, 33014 Tampere, Finland.
The Immunopharmacology Research Group, School of Medicine, University of Tampere and Tampere University Hospital, 33014 Tampere, Finland ; Allergy Centre, Tampere University Hospital, PL 2000, 33521 Tampere, Finland.
Mediators Inflamm. 2014;2014:232167. doi: 10.1155/2014/232167. Epub 2014 May 6.
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.
COPD(慢性阻塞性肺疾病)是一种常见的肺部疾病,其特征是气流受限和全身炎症。最近,脂肪组织介导的炎症在疾病发病机制中的作用引起了越来越多的关注。在这项研究中,我们通过测量它们是否与炎症活动、肺功能或症状相关,来研究新型脂肪细胞因子 nesfatin-1 和 visfatin 在 COPD 中的作用。我们测量了 43 名男性肺气肿性 COPD 患者的血浆 NUCB2/nesfatin-1 和 visfatin 水平以及白细胞介素-6 (IL-6)、白细胞介素-8 (IL-8)、肿瘤坏死因子-α (TNF-α)和基质金属蛋白酶-9 (MMP-9),同时还测量了肺功能、呼气一氧化氮和症状。在 4 周吸入氟替卡松治疗后,对患者亚组重复了这些测量。Visfatin 和 NUCB2/nesfatin-1 与血浆中 IL-6(r = 0.341,P = 0.027 和 rho = 0.401,P = 0.008,分别)和 TNF-α(r = 0.305,P = 0.052 和 rho = 0.329,P = 0.033,分别)呈正相关,在 COPD 患者中,NUCB2/nesfatin-1 也与 IL-8(rho = 0.321,P = 0.036)呈正相关。此外,血浆 visfatin 水平与肺弥散能力呈负相关(r = -0.369,P = 0.016)。脂肪细胞因子在氟替卡松治疗中均不受影响,与类固醇反应性无关。本研究结果表明,脂肪细胞因子 NUCB2/nesfatin-1 和 visfatin 是与 COPD 全身炎症相关的新型因素,并提示 visfatin 可能介导肺弥散能力受损。