Journal
JOURNAL OF CYSTIC FIBROSIS
Volume 17, Issue 5, Pages 607-615Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jcf.2017.11.017
Keywords
Resolvin D1; Airway surface liquid layer; ENaC; F508del-CFTR; CF mice; CF alveolar macrophages
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Funding
- Institut National de la Sante et de la Recherche Medicate (INSEAM, France)
- Vaincre la Mucoviscidose (VLM, France) [RF20150501364/1/1/50]
- National Children's Research Center (NCRC, Ireland, TRAPCF project)
- EU BMBS COST Action [BM1003]
- Health Research Board of Ireland (HRB) [HRA/POR/2011/21 - 1403]
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Background: Cystic Fibrosis (CF) lung disease is characterised by dysregulated ion transport that promotes chronic bacterial infection and inflammation. The impact of the specialised pro-resolution mediator resolvin D1 (RvD1) on airway surface liquid (ASL) dynamics and innate defence had not yet been investigated in CF airways. Methods: Ex vivo studies were performed on primary cultures of alveolar macrophages and bronchial epithelial cells from children with CF and in human bronchial epithelial cell lines; in vivo studies were performed in homozygous F508del-CFTR mice treated with vehicle control or RvD1 (1-100 nM). Results: RvD1 increased the CF ASL height in human bronchial epithelium and restored the nasal trans-epithelial potential difference in CF mice by decreasing the amiloride-sensitive Na+ absorption and stimulating CFTR-independent Cl- secretion. RvD1 decreased TNF alpha induced IL-8 secretion and enhanced the phagocytic and bacterial killing capacity of human CF alveolar macrophages. Conclusion: RvD1 resolves CF airway pathogenesis and has therapeutic potential in CF lung disease. (C) 2017 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.
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