- Title
- Airway β-defensin-1 protein Is elevated in COPD and severe asthma
- Creator
- Baines, Katherine J.; Wright, Thomas K.; Simpson, Jodie L.; McDonald, Vanessa M.; Wood, Lisa G.; Parsons, Kristy S.; Wark, Peter A.; Gibson, Peter G.
- Relation
- NHMRC.1045371
- Relation
- Mediators of Inflammation Vol. 2015
- Publisher Link
- http://dx.doi.org/10.1155/2015/407271
- Publisher
- Hindawai Publishing
- Resource Type
- journal article
- Date
- 2015
- Description
- 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.
- Subject
- antimicrobial peptides; β-defensin-1; chronic obstructive pulmonary disease (COPD); asthma
- Identifier
- http://hdl.handle.net/1959.13/1313952
- Identifier
- uon:22673
- Identifier
- ISSN:0962-9351
- Language
- eng
- Full Text
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