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CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis
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...
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Published in: | Journal of cystic fibrosis 2017-07, Vol.16 (4), p.475-482 |
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creator | Tarique, Abdullah A Sly, Peter D Holt, Patrick G Bosco, Anthony Ware, Robert S Logan, Jayden Bell, Scott C Wainwright, Claire E Fantino, Emmanuelle |
description | 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. |
doi_str_mv | 10.1016/j.jcf.2017.03.011 |
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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.</description><identifier>ISSN: 1569-1993</identifier><identifier>EISSN: 1873-5010</identifier><identifier>DOI: 10.1016/j.jcf.2017.03.011</identifier><identifier>PMID: 28428011</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adult ; Alternatively activated macrophages ; CFTR ; CFTR inhibitors ; Child ; Classically activated macrophages ; Cystic fibrosis (CF) ; Cystic Fibrosis - immunology ; Cystic Fibrosis - pathology ; Cystic Fibrosis - physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator - genetics ; Endocytosis ; Female ; Humans ; IL-13 receptor ; Inflammation - immunology ; Interleukin-13 - immunology ; Interleukin-13 Receptor alpha1 Subunit - immunology ; Interleukin-4 - immunology ; Lung - immunology ; Lung - pathology ; Lung - physiopathology ; Macrophage Activation - immunology ; Macrophages - immunology ; Macrophages - pathology ; Male ; Monocyte-derived macrophages ; Phagocytosis ; Pulmonary/Respiratory</subject><ispartof>Journal of cystic fibrosis, 2017-07, Vol.16 (4), p.475-482</ispartof><rights>European Cystic Fibrosis Society.</rights><rights>2017 European Cystic Fibrosis Society</rights><rights>Copyright © 2017 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-87f9c2717fb164f67be51273e4c18284dafef26d6e202b8cd5827ce26b5098793</citedby><cites>FETCH-LOGICAL-c451t-87f9c2717fb164f67be51273e4c18284dafef26d6e202b8cd5827ce26b5098793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28428011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tarique, Abdullah A</creatorcontrib><creatorcontrib>Sly, Peter D</creatorcontrib><creatorcontrib>Holt, Patrick G</creatorcontrib><creatorcontrib>Bosco, Anthony</creatorcontrib><creatorcontrib>Ware, Robert S</creatorcontrib><creatorcontrib>Logan, Jayden</creatorcontrib><creatorcontrib>Bell, Scott C</creatorcontrib><creatorcontrib>Wainwright, Claire E</creatorcontrib><creatorcontrib>Fantino, Emmanuelle</creatorcontrib><title>CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis</title><title>Journal of cystic fibrosis</title><addtitle>J Cyst Fibros</addtitle><description>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.</description><subject>Adult</subject><subject>Alternatively activated macrophages</subject><subject>CFTR</subject><subject>CFTR inhibitors</subject><subject>Child</subject><subject>Classically activated macrophages</subject><subject>Cystic fibrosis (CF)</subject><subject>Cystic Fibrosis - immunology</subject><subject>Cystic Fibrosis - pathology</subject><subject>Cystic Fibrosis - physiopathology</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</subject><subject>Endocytosis</subject><subject>Female</subject><subject>Humans</subject><subject>IL-13 receptor</subject><subject>Inflammation - immunology</subject><subject>Interleukin-13 - immunology</subject><subject>Interleukin-13 Receptor alpha1 Subunit - immunology</subject><subject>Interleukin-4 - immunology</subject><subject>Lung - immunology</subject><subject>Lung - pathology</subject><subject>Lung - physiopathology</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Monocyte-derived macrophages</subject><subject>Phagocytosis</subject><subject>Pulmonary/Respiratory</subject><issn>1569-1993</issn><issn>1873-5010</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kUtLxDAQx4Movj-AF-nRS2smfSRFEGTxBYLg4xzSZKKp3XZNugv77U1Z9eDB08zhN39mfkPICdAMKFTnbdZqmzEKPKN5RgG2yD4InqclBbod-7KqU6jrfI8chNDSCFIudskeEwUTkd8nj7Obl6fU4AJ7g_2YGLSox8T1iepG9L0a3Qq7dap0bNSIJpkr7YfFu3rDMGF6HUanE-saPwQXjsiOVV3A4-96SF5vrl9md-nD4-397Ooh1UUJYyq4rTXjwG0DVWEr3mAJjOdYaBBxO6MsWlaZChlljdCmFIxrZFVT0lrwOj8kZ5vchR8-lxhGOXdBY9epHodlkCBqABajIKKwQePeIXi0cuHdXPm1BConj7KV0aOcPEqay-glzpx-xy-bOZrfiR9xEbjYABiPXDn0MmiHvUbjfBQozeD-jb_8M6071zutug9cY2iHZTTfxStkYJLK5-mR0x-B55TWBcu_ACB2l5c</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Tarique, Abdullah A</creator><creator>Sly, Peter D</creator><creator>Holt, Patrick G</creator><creator>Bosco, Anthony</creator><creator>Ware, Robert S</creator><creator>Logan, Jayden</creator><creator>Bell, Scott C</creator><creator>Wainwright, Claire E</creator><creator>Fantino, Emmanuelle</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170701</creationdate><title>CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis</title><author>Tarique, Abdullah A ; Sly, Peter D ; Holt, Patrick G ; Bosco, Anthony ; Ware, Robert S ; Logan, Jayden ; Bell, Scott C ; Wainwright, Claire E ; Fantino, Emmanuelle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-87f9c2717fb164f67be51273e4c18284dafef26d6e202b8cd5827ce26b5098793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Alternatively activated macrophages</topic><topic>CFTR</topic><topic>CFTR inhibitors</topic><topic>Child</topic><topic>Classically activated macrophages</topic><topic>Cystic fibrosis (CF)</topic><topic>Cystic Fibrosis - immunology</topic><topic>Cystic Fibrosis - pathology</topic><topic>Cystic Fibrosis - physiopathology</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</topic><topic>Endocytosis</topic><topic>Female</topic><topic>Humans</topic><topic>IL-13 receptor</topic><topic>Inflammation - immunology</topic><topic>Interleukin-13 - immunology</topic><topic>Interleukin-13 Receptor alpha1 Subunit - immunology</topic><topic>Interleukin-4 - immunology</topic><topic>Lung - immunology</topic><topic>Lung - pathology</topic><topic>Lung - physiopathology</topic><topic>Macrophage Activation - immunology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Monocyte-derived macrophages</topic><topic>Phagocytosis</topic><topic>Pulmonary/Respiratory</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tarique, Abdullah A</creatorcontrib><creatorcontrib>Sly, Peter D</creatorcontrib><creatorcontrib>Holt, Patrick G</creatorcontrib><creatorcontrib>Bosco, Anthony</creatorcontrib><creatorcontrib>Ware, Robert S</creatorcontrib><creatorcontrib>Logan, Jayden</creatorcontrib><creatorcontrib>Bell, Scott C</creatorcontrib><creatorcontrib>Wainwright, Claire E</creatorcontrib><creatorcontrib>Fantino, Emmanuelle</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cystic fibrosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tarique, Abdullah A</au><au>Sly, Peter D</au><au>Holt, Patrick G</au><au>Bosco, Anthony</au><au>Ware, Robert S</au><au>Logan, Jayden</au><au>Bell, Scott C</au><au>Wainwright, Claire E</au><au>Fantino, Emmanuelle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis</atitle><jtitle>Journal of cystic fibrosis</jtitle><addtitle>J Cyst Fibros</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>16</volume><issue>4</issue><spage>475</spage><epage>482</epage><pages>475-482</pages><issn>1569-1993</issn><eissn>1873-5010</eissn><abstract>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.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28428011</pmid><doi>10.1016/j.jcf.2017.03.011</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Alternatively activated macrophages CFTR CFTR inhibitors Child Classically activated macrophages Cystic fibrosis (CF) Cystic Fibrosis - immunology Cystic Fibrosis - pathology Cystic Fibrosis - physiopathology Cystic Fibrosis Transmembrane Conductance Regulator - genetics Endocytosis Female Humans IL-13 receptor Inflammation - immunology Interleukin-13 - immunology Interleukin-13 Receptor alpha1 Subunit - immunology Interleukin-4 - immunology Lung - immunology Lung - pathology Lung - physiopathology Macrophage Activation - immunology Macrophages - immunology Macrophages - pathology Male Monocyte-derived macrophages Phagocytosis Pulmonary/Respiratory |
title | CFTR-dependent defect in alternatively-activated macrophages in cystic fibrosis |
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