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Azithromycin increases chloride efflux from cystic fibrosis airway epithelial cells
Uppsala University, Sweden.
Uppsala University, Sweden.
Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden.
Uppsala University, Sweden.
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2009 (Engelska)Ingår i: Experimental Lung Research, ISSN 0190-2148, E-ISSN 1521-0499, Vol. 35, nr 3, 210-221 s.Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

It was investigated whether azithromycin (AZM) stimulates chloride (Cl-) efflux from cystic fibrosis (CF) and non-CF airway epithelial cells, possibly secondary to up-regulation of the multidrug resistance protein (MDR). CF and non-CF human airway epithelial cell lines (CFBE and 16HBE) were treated with 0.4, 4, and 40 microg/mL AZM for 4 days. Cl- efflux was explored in the presence or absence of specific inhibitors of CFTR and alternative Cl- channels. Six CF patients received AZM (500 mg daily) for 6 months. The percentage of predicted forced vital capacity (FVC%), forced expiratory volume (FEV1%), and the number of acute exacerbations were compared before and after treatment. Nasal biopsies were taken before and after treatment, and mRNA expression of MDR and CFTR was determined by in situ hybridization. A significant dose-dependent increase of Cl- efflux from CFBE cells (but not from 16HBE cells) was observed after AZM treatment. A CFTR inhibitor significantly reduced AZM-stimulated Cl- efflux from CFBE cells. A significant improvement in FEV1%, and fewer exacerbations were observed. AZM treatment did not affect mRNA expression of MDR and CFTR. The stimulation of Cl- efflux could be part of the explanation for the clinical improvement seen among the patients.

Ort, förlag, år, upplaga, sidor
Informa Healthcare, 2009. Vol. 35, nr 3, 210-221 s.
Nyckelord [en]
azithromycin, chloride transport, cystic fibrosis transmembrane conductance regulator, cystic fibrosis, lung function, multidrug resistance
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-102548DOI: 10.1080/01902140802534967PubMedID: 19337904OAI: oai:DiVA.org:liu-102548DiVA: diva2:678973
Tillgänglig från: 2013-12-13 Skapad: 2013-12-13 Senast uppdaterad: 2017-12-06Bibliografiskt granskad

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