Literature DB >> 28428011

CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis.

Abdullah A Tarique1, Peter D Sly2, Patrick G Holt3, Anthony Bosco4, Robert S Ware1, Jayden Logan1, Scott C Bell5, Claire E Wainwright6, Emmanuelle Fantino1.   

Abstract

BACKGROUND: The role of the macrophages in cystic fibrosis (CF) lung disease has been poorly studied. We hypothesized that alternatively activated M2 macrophages are abnormal in CF lung disease.
METHODS: Blood samples were collected from adults (n=13) children (n=27) with CF on admission for acute pulmonary exacerbation and when clinically stable. Monocytes were differentiated into macrophages and polarized into classical (M1) and alternatively-activated (M2) phenotypes, function determined ex-vivo and compared with healthy controls.
RESULTS: In the absence of functional cystic fibrosis trans-membrane conductance regulator (CFTR), either naturally in patients with CF or induced with CFTR inhibitors, monocyte-derived macrophages do not respond to IL-13/IL-4, fail to polarize into M2s associated with a post-transcriptional failure to produce and express IL-13Rα1 on the macrophage surface Polarization to the M1 phenotype was unaffected.
CONCLUSIONS: CFTR-dependent imbalance of macrophage phenotypes and functions could contribute to the exaggerated inflammatory response seen in CF lung disease.
Copyright © 2017 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Alternatively activated macrophages); CFTR; CFTR inhibitors; Classically activated macrophages; Cystic fibrosis (CF); Endocytosis; IL-13 receptor; Monocyte-derived macrophages; Phagocytosis

Mesh:

Substances:

Year:  2017        PMID: 28428011     DOI: 10.1016/j.jcf.2017.03.011

Source DB:  PubMed          Journal:  J Cyst Fibros        ISSN: 1569-1993            Impact factor:   5.482


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