Airway β-Defensin-1 Protein Is Elevated in COPD and Severe Asthma

• Main Authors: Katherine J. Baines (Author), Thomas K. Wright (Author), Jodie L. Simpson (Author), Vanessa M. McDonald (Author), Lisa G. Wood (Author), Kristy S. Parsons (Author), Peter A. Wark (Author), Peter G. Gibson (Author)
• Format: Book
• Published: Hindawi Limited, 2015-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

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.

Item Description

0962-9351
1466-1861
10.1155/2015/407271