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A small molecule neutrophil elastase inhibitor, KRP-109, inhibits cystic fibrosis mucin degradation.
J. Cyst. Fibros. 15, 325-331 (2016)
Publ. Version/Full Text
Research data
DOI
PMC
BACKGROUND: Neutrophil elastase (NE) rapidly degrades gel-forming airway mucins in cystic fibrosis (CF) sputum. We hypothesized that KRP-109, a small molecule NE inhibitor, would inhibit CF mucin degradation in vitro. METHODS: Sputa were collected from CF patients (n=5) chronically or intermittently infected with Pseudomonas aeruginosa (P.a.). Mucin degradation was analyzed using western blot. Protease inhibitor studies were performed using alpha1-proteinase inhibitor (A1-PI Prolastin®) and KRP-109. Elastase activity assays were performed using spectrophotometry. RESULTS: There were significant differences in the amount of active NE in different CF sputum samples. KRP-109 decreased the NE driven mucin degradation in vitro. Pseudomonas elastases appeared to blunt elastase inhibition by A1-PI or KRP-109. CONCLUSION: Inhibitors of neutrophil and Pseudomonas-derived elastases might rescue mucus clearance and reverse airway obstruction in CF.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cystic Fibrosis ; Mucin ; Protease And Anti-protease Balance ; Small Molecule Inhibitors; Lung-disease; Pseudomonas-aeruginosa; Alpha-1-proteinase Inhibitor; Iron Homeostasis; Proteases; Inflammation; Efficacy; Alpha(1)-antitrypsin; Safety; Antiproteases
ISSN (print) / ISBN
1569-1993
e-ISSN
1873-5010
Journal
Journal of Cystic Fibrosis
Quellenangaben
Volume: 15,
Issue: 3,
Pages: 325-331
Publisher
Elsevier
Publishing Place
Amsterdam
Reviewing status
Peer reviewed
Institute(s)
Institute of Lung Health and Immunity (LHI)