期刊
EXPERIMENTAL LUNG RESEARCH
卷 36, 期 6, 页码 373-380出版社
TAYLOR & FRANCIS INC
DOI: 10.3109/01902141003690389
关键词
airway epithelium; airway markers; chronic obstructive pulmonary disease; interstitial lung disease
Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) may be caused by epithelial cell injury. Epithelial cells respond to injury by secreting innate immunity proteins. To investigate whether altered levels of innate immunity proteins are observed in COPD and IPF, the authors assessed secretory leukocyte protease inhibitor (SLPI), elafin, CC16, and beta-defensin-2 levels by enzyme-linked immunosorbent assay (ELISA) in sputum supernatants from COPD patients (n = 19), smokers without COPD (n = 21), and never-smokers (n = 10) and in BALF supernatants from patients with IPF (n = 11) and subjects without IPF (n = 11). CC16 levels were decreased, whereas SLPI and elafin levels were increased in COPD patients (0.8 [0-4.2] mu g/mL, 2.5 [0.3-10.5] mu g/mL, 213 [152-318] pg/mL, respectively) compared to smokers without COPD (1.8 [0.1-21.2] mu g/mL, 0.8 [0.2-2.6] mu g/mL, 172 [71-473] pg/mL, respectively) and never-smokers (0.5 [0-4.8] mu g/mL, 0.1 [0.05-0.6] mu g/mL, 188 [129-218] pg/mL, respectively) (CC16: P = .001; SLPI: P < .001; elafin: P = .041). beta-Defensin-2 was detected in smokers without COPD (98 [10-729] pg/mL) and never-smokers (74 [35-410] pg/mL), but not in COPD. SLPI and elafin levels did not differ between IPF patients and controls, but CC16 levels were increased in IPF (0.5 [0-2.3] versus 0.2 [0-0.3] mu g/mL; P = .019). beta-Defensin-2 was not detected in BALF. In conclusion, in COPD, secretion of CC16 and beta-defensin-2 might be suppressed, whereas SLPI and elafin secretion is up-regulated. In IPF, only CC16 secretion is up-regulated.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据