Broekhuizen R, Vernooy J H J, Schols A M W J, Dentener M A, Wouters E F M
Department of Respiratory Medicine, Nutrition and Toxicology Research Institute Maastricht, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.
Respir Med. 2005 Jan;99(1):70-4. doi: 10.1016/j.rmed.2004.03.029.
Chronic inflammation of the lung is a characteristic finding in chronic obstructive pulmonary disease (COPD). Leptin is a pleiotropic cytokine thought to play a role in host response to inflammation. As recent studies have shown that leptin receptors are present in the lung, this study aimed to determine if leptin is detectable in induced sputum of COPD patients and if there is a relationship between leptin and other inflammatory markers in sputum.
Sputum was induced in 14 male patients with moderate COPD (FEV1: 56 (15) % pred.). Leptin, total tumour necrosis factor (TNF)-alpha, and C-reactive protein (CRP) were analyzed in induced sputum supernatant by ELISA. Leptin was also determined in EDTA plasma.
Leptin was detectable in induced sputum of 10 COPD patients. A significant relationship was found between sputum leptin and CRP (r = 0.943, P < 0.001) and total TNF-alpha (r = 0.690, P < 0.01). Plasma leptin and sputum leptin were inversely correlated (r = -0.643, P < 0.01).
The present study demonstrated that leptin is detectable in induced sputum of patients with moderate COPD and is related to other inflammatory markers. The observed correlations between leptin and inflammatory markers in sputum may indicate that leptin is involved in the local inflammatory response in COPD.
肺部慢性炎症是慢性阻塞性肺疾病(COPD)的一个典型特征。瘦素是一种多效性细胞因子,被认为在宿主对炎症的反应中发挥作用。由于最近的研究表明肺中存在瘦素受体,本研究旨在确定COPD患者诱导痰中是否可检测到瘦素,以及瘦素与痰中其他炎症标志物之间是否存在关联。
对14例中度COPD男性患者(FEV1:56(15)%预计值)进行痰液诱导。通过酶联免疫吸附测定法(ELISA)分析诱导痰上清液中的瘦素、总肿瘤坏死因子(TNF)-α和C反应蛋白(CRP)。还测定了乙二胺四乙酸(EDTA)血浆中的瘦素。
10例COPD患者的诱导痰中可检测到瘦素。发现痰瘦素与CRP(r = 0.943,P < 0.001)和总TNF-α(r = 0.690,P < 0.01)之间存在显著相关性。血浆瘦素与痰瘦素呈负相关(r = -0.643,P < 0.01)。
本研究表明,中度COPD患者的诱导痰中可检测到瘦素,且其与其他炎症标志物有关。观察到的痰中瘦素与炎症标志物之间的相关性可能表明瘦素参与了COPD的局部炎症反应。