Innate immunity proteins in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis

• Published in: Experimental lung research Vol. 36; no. 6; pp. 373 - 380
• Main Authors: Tsoumakidou, Maria, Bouloukaki, Izolde, Thimaki, Katerina, Tzanakis, Nikos, Siafakas, Nikos M.
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.07.2010; Taylor & Francis
• Subjects: Adult; Aged; airway epithelium; airway markers; beta-Defensins - analysis; Biomarkers - analysis; Bronchoalveolar Lavage Fluid - immunology; chronic obstructive pulmonary disease; Elafin - analysis; Enzyme-Linked Immunosorbent Assay; Female; Greece; Humans; Idiopathic Pulmonary Fibrosis - immunology; Immunity, Innate; interstitial lung disease; Male; Middle Aged; Pulmonary Disease, Chronic Obstructive - immunology; Respiratory Mucosa - immunology; Secretory Leukocyte Peptidase Inhibitor - analysis; Smoking - immunology; Smoking Cessation; Sputum - immunology; Uteroglobin - analysis; Young Adult; Greece
• ISSN: 0190-2148; 1521-0499; 1521-0499
• DOI: 10.3109/01902141003690389

ABSTRACT 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 β-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] μg/mL, 2.5 [0.3-10.5] μg/mL, 213 [152-318] pg/mL, respectively) compared to smokers without COPD (1.8 [0.1-21.2] μg/mL, 0.8 [0.2-2.6] μg/mL, 172 [71-473] pg/mL, respectively) and never-smokers (0.5 [0-4.8] μg/mL, 0.1 [0.05-0.6] μg/mL, 188 [129-218] pg/mL, respectively) (CC16: P = .001; SLPI: P <.001; elafin: P = .041). β-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] μg/mL; P = .019). β-Defensin-2 was not detected in BALF. In conclusion, in COPD, secretion of CC16 and β-defensin-2 might be suppressed, whereas SLPI and elafin secretion is up-regulated. In IPF, only CC16 secretion is up-regulated.