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dc.contributor.authorSu, Yung-Changen_US
dc.contributor.authorS. Rolph, Michaelen_US
dc.contributor.authorG. Hansbro, Nicoleen_US
dc.contributor.authorMackay, Charles R.en_US
dc.contributor.authorA. Sewell, Williamen_US
dc.date.accessioned2017-04-24T13:39:49Z
dc.date.available2017-04-24T13:39:49Z
dc.date.issued2008en_US
dc.date.modified2011-09-15T05:46:24Z
dc.identifier.issn00221767en_US
dc.identifier.urihttp://hdl.handle.net/10072/38561
dc.description.abstractGM-CSF plays an important role in inflammation by promoting the production, activation, and survival of granulocytes and macrophages. In this study, GM-CSF knockout (GM-CSF-/-) mice were used to investigate the role of GM-CSF in a model of allergic airway inflammation. In allergic GM-CSF-/- mice, eosinophil recruitment to the airways showed a striking pattern, with eosinophils present in perivascular areas, but almost completely absent in peribronchial areas, whereas in wild-type mice, eosinophil infiltration appeared in both areas. In the GM-CSF-/- mice, mucus production in the airways was also reduced, and eosinophil numbers were markedly reduced in the bronchoalveolar lavage (BAL)3 fluid. IL-5 production was reduced in the lung tissue and BAL fluid of GM-CSF-/- mice, but IL-4 and IL-13 production, airway hyperresponsiveness, and serum IgE levels were not affected. The presence of eosinophils in perivascular but not peribronchial regions was suggestive of a cell migration defect in the airways of GM-CSF-/- mice. The CCR3 agonists CCL5 (RANTES) and CCL11 (eotaxin-1) were expressed at similar levels in GM-CSF-/- and wild-type mice. However, IFN-? mRNA and protein were increased in the lung tissue and BAL fluid in GM-CSF-/- mice, as were mRNA levels of the IFN-?-inducible chemokines CXCL9 (Mig), CXCL10 (IP-10), and CXCL11 (I-Tac). Interestingly, these IFN-?-inducible chemokines are natural antagonists of CCR3, suggesting that their overproduction in GM-CSF-/- mice contributes to the lack of airway eosinophils. These findings demonstrate distinctive abnormalities to a model of allergic asthma in the absence of GM-CSF.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherAmerican Association of Immunologistsen_US
dc.publisher.placeUnited Statesen_US
dc.publisher.urihttp://www.jimmunol.org/content/180/4/2600.shorten_AU
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom2600en_US
dc.relation.ispartofpageto2607en_US
dc.relation.ispartofissue4en_US
dc.relation.ispartofjournalJournal of Immunologyen_US
dc.relation.ispartofvolume180en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchAllergyen_US
dc.subject.fieldofresearchcode110701en_US
dc.titleGranulocyte-macrophage colony-stimulating factor is required for bronchial eosinophilia in a murine model of allergic airway inflammationen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_AU
gro.date.issued2008
gro.hasfulltextNo Full Text


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