Antimicrobial Peptides SLPI and Beta Defensin-1 in Sputum are Negatively Correlated with FEV


Journal

International journal of chronic obstructive pulmonary disease
ISSN: 1178-2005
Titre abrégé: Int J Chron Obstruct Pulmon Dis
Pays: New Zealand
ID NLM: 101273481

Informations de publication

Date de publication:
Historique:
received: 13 01 2021
accepted: 19 04 2021
entrez: 7 6 2021
pubmed: 8 6 2021
medline: 28 7 2021
Statut: epublish

Résumé

Chronic obstructive pulmonary disease (COPD) and asthma have heterogeneous inflammation with inhaled corticosteroids (ICS) as a mainstay of treatment. There is increased prevalence of non-typeable Secretory leukocyte protease inhibitor (SLPI), osteopontin, elafin and beta defensin-1 were measured in sputum supernatants from healthy donors (n=9), asthmatics (n=21) and patients with COPD (n=14). Elafin and beta defensin-1 were measured in a primary human bronchial epithelial cells (HBECs) from healthy and COPD donors infected with NTHi and pre-treated with fluticasone propionate (FP) and budesonide (BUD). Internalised NTHi was quantified by qPCR. Sputum SLPI was negatively correlated with FEV1 (p<0.001, r=-0.610), FEV1% predicted (p<0.001, r=-0.583) and FEV1/FVC (p=0.001, r=-0.528). Sputum beta defensin-1 was negatively associated with FEV1 (p<0.001***r=-0.594). SLPI and beta defensin-1 levels in sputum were higher in the healthy controls and COPD group compared to the asthma group (p=0.001 and p=0.014) and (p<0.001 and p=0.007, respectively). ICS use was associated with higher sputum osteopontin compared to those with no ICS use. NTHi infection of COPD HBECs produced higher levels of beta defensin-1 compared to healthy donors (mean (SD) release: 45.1pg/mL (7.3) vs 21.2pg/mL (7.3) respectively, p=0.014). Elafin release from HBECs from COPD donors did not change following NTHi infection; however, elafin from healthy donors was significantly reduced (%mean reduction: 23.7%, 95% confidence intervals (CI) of reduction: 5.3-38.4%, p<0.01). Sputum SLPI and beta defensin-1 may be markers to identify those patients with declining lung function. ICS use was associated with higher sputum osteopontin compared to those with no ICS use.

Sections du résumé

BACKGROUND BACKGROUND
Chronic obstructive pulmonary disease (COPD) and asthma have heterogeneous inflammation with inhaled corticosteroids (ICS) as a mainstay of treatment. There is increased prevalence of non-typeable
METHODS METHODS
Secretory leukocyte protease inhibitor (SLPI), osteopontin, elafin and beta defensin-1 were measured in sputum supernatants from healthy donors (n=9), asthmatics (n=21) and patients with COPD (n=14). Elafin and beta defensin-1 were measured in a primary human bronchial epithelial cells (HBECs) from healthy and COPD donors infected with NTHi and pre-treated with fluticasone propionate (FP) and budesonide (BUD). Internalised NTHi was quantified by qPCR.
RESULTS RESULTS
Sputum SLPI was negatively correlated with FEV1 (p<0.001, r=-0.610), FEV1% predicted (p<0.001, r=-0.583) and FEV1/FVC (p=0.001, r=-0.528). Sputum beta defensin-1 was negatively associated with FEV1 (p<0.001***r=-0.594). SLPI and beta defensin-1 levels in sputum were higher in the healthy controls and COPD group compared to the asthma group (p=0.001 and p=0.014) and (p<0.001 and p=0.007, respectively). ICS use was associated with higher sputum osteopontin compared to those with no ICS use. NTHi infection of COPD HBECs produced higher levels of beta defensin-1 compared to healthy donors (mean (SD) release: 45.1pg/mL (7.3) vs 21.2pg/mL (7.3) respectively, p=0.014). Elafin release from HBECs from COPD donors did not change following NTHi infection; however, elafin from healthy donors was significantly reduced (%mean reduction: 23.7%, 95% confidence intervals (CI) of reduction: 5.3-38.4%, p<0.01).
CONCLUSION CONCLUSIONS
Sputum SLPI and beta defensin-1 may be markers to identify those patients with declining lung function. ICS use was associated with higher sputum osteopontin compared to those with no ICS use.

Identifiants

pubmed: 34093009
doi: 10.2147/COPD.S301622
pii: 301622
pmc: PMC8170372
doi:

Substances chimiques

Pore Forming Cytotoxic Proteins 0
SLPI protein, human 0
Secretory Leukocyte Peptidase Inhibitor 0
beta-Defensins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1437-1447

Informations de copyright

© 2021 Cane et al.

Déclaration de conflit d'intérêts

The authors declare that they have no competing interests.

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Auteurs

Jennifer Cane (J)

Respiratory Medicine Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Oxford NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.

Laura Tregidgo (L)

Respiratory Medicine Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Samantha Thulborn (S)

Respiratory Medicine Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Oxford NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.

Donna Finch (D)

Alchemab Therapeutics, Cambridge, UK.

Mona Bafadhel (M)

Respiratory Medicine Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Oxford NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.

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Classifications MeSH