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

Abstract EN

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.