Evidence map›Paper›PMID 26568662›Full record

ArticleMediators of inflammation2015

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

Katherine J Baines, Thomas K Wright, Jodie L Simpson, Vanessa M McDonald, Lisa G Wood, Kristy S Parsons, Peter A Wark, Peter G Gibson

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026
    Review
  2. Article
  3. E-Cigarette Use, Cigarette Smoking, and Sex Are Associated With Nasal Microbiome Dysbiosis.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Protective effects of ΔBritish journal of pharmacology · 2020
    Article
  10. Expression and Function of Host Defense Peptides at Inflammation Sites.International journal of molecular sciences · 2019
    Review
  11. Regulation of IL-17A and implications for TGF-β1 comodulation of airway smooth muscle remodeling in severe asthma.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  12. Article
  13. At the Root: Defining and Halting Progression of Early Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2018
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Antimicrobial Peptides SLPI and Beta Defensin-1 in Sputum are Negatively Correlated with FEVInternational journal of chronic obstructive pulmonary disease
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Katherine J BainesPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Thomas K WrightPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Jodie L SimpsonPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Vanessa M McDonaldPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Lisa G WoodPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Kristy S ParsonsPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Peter A WarkPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
Peter G GibsonPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, New Lambton Heights, NSW 2305, Australia ; Department of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, NSW 2305, Australia.
John Hunter Hospital · AUHunter Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInnate 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.

methodsInduced 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).

resultsAirway 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.

conclusionsElevated 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.

Indexed as

AdultAgedAsthmabeta-DefensinsCells, CulturedFemaleHumansMaleMiddle AgedPulmonary Disease, Chronic Obstructivebeta-DefensinsDEFB1 protein, human

Identifiers

PMID26568662
PMCPMC4629049
OpenAlexW2103552948

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.