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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.

Airwayβ-Defensin-1 Protein Is Elevated in COPD and Severe Asthma