In:
Mediators of Inflammation, Hindawi Limited, Vol. 2015 ( 2015), p. 1-8
Abstract:
Background . Innate immune antimicrobial peptides, including β -defensin-1, promote the chemotaxis and activation of several immune cells. The role of β -defensin-1 in asthma and chronic obstructive pulmonary disease (COPD) remains unclear. Methods . Induced sputum was collected from healthy controls and individuals with asthma or COPD. β -defensin-1 protein in sputum supernatant was quantified by ELISA. Biomarker potential was examined using receiver operating characteristic curves. β -defensin-1 release from primary bronchial epithelial cells (pBECs) was investigated in culture with and without cigarette smoke extract (CSE). Results . Airway β -defensin-1 protein was elevated in COPD participants compared to asthma participants and healthy controls. Inflammatory phenotype had no effect on β -defensin-1 levels in asthma or COPD. β -defensin-1 protein was significantly higher in severe asthma compared to controlled and uncontrolled asthma. β -defensin-1 protein could predict the presence of COPD from both healthy controls and asthma patients. Exposure of pBECs to CSE decreased β -defensin-1 production in healthy controls; however in pBECs from COPD participants the level of β -defensin-1 remanied unchanged. Conclusions . Elevated β -defensin-1 protein is a feature of COPD and severe asthma regardless of inflammatory phenotype. β -defensin-1 production is dysregulated in the epithelium of patients with COPD and may be an effective biomarker and potential therapeutic target.
Type of Medium:
Online Resource
ISSN:
0962-9351
,
1466-1861
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2015
detail.hit.zdb_id:
2008065-7
