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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-17T12:05:31Z</responseDate> <request identifier=oai:HAL:hal-01560280v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01560280v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-SMS</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:IRSET-3</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:IRSET-EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>The impact of impaired macrophage functions in cystic fibrosis disease progression</title> <creator>Lévêque, Manuella</creator> <creator>Le Trionnaire, Sophie</creator> <creator>Del Porto, Paola</creator> <creator>Martin-Chouly, Corinne</creator> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Department of Biology and Biotechnology "Charles Darwin" ; Università degli Studi di Roma "La Sapienza" [Rome]</contributor> <contributor>This work was supported by ‘Vaincre La Mucoviscidose’ (French Cystic Fibrosis Association) [grant number RF20130500807] and ‘Region Bretagne’ [grant number SAD MUCOREMI 8209].</contributor> <description>International audience</description> <source>ISSN: 1569-1993</source> <source>Journal of Cystic Fibrosis</source> <publisher>Elsevier</publisher> <identifier>hal-01560280</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560280</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560280/document</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560280/file/Chouly-The%20impact%20of%20impaired%20macrophage%20functions.pdf</identifier> <source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560280</source> <source>Journal of Cystic Fibrosis, Elsevier, 2017, 16 (4), pp.443-453. 〈10.1016/j.jcf.2016.10.011〉</source> <identifier>DOI : 10.1016/j.jcf.2016.10.011</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.jcf.2016.10.011</relation> <identifier>PUBMED : 27856165</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/27856165</relation> <language>en</language> <subject lang=en>Cystic fibrosis</subject> <subject lang=en> Inflammation</subject> <subject lang=en> Lipid homeostasis</subject> <subject lang=en> Macrophage</subject> <subject lang=en> Phagocytosis</subject> <subject>[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract</subject> <subject>[SDV.IMM] Life Sciences [q-bio]/Immunology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>The underlying cause of morbidity in cystic fibrosis (CF) is the decline in lung function, which results in part from chronic inflammation. Inflammation and infection occur early in infancy in CF and the role of innate immune defense in CF has been highlighted in the last years. Once thought simply to be consumers of bacteria, macrophages have emerged as highly sensitive immune cells that are located at the balance point between inflammation and resolution of this inflammation in CF pathophysiology. In order to assess the potential role of macrophage in CF, we review the evidence that: (1) CF macrophage has a dysregulated inflammatory phenotype; (2) CF macrophage presents altered phagocytosis capacity and bacterial killing; and (3) lipid disorders in CF macrophage affect its function. These alterations of macrophage weaken innate defense of CF patients and may be involved in CF disease progression and lung damage.</description> <date>2017</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>