dc.contributor.author | Su, Yung-Chang | |
dc.contributor.author | Rolph, Michael S. | |
dc.contributor.author | Hansbro, Nicole G. | |
dc.contributor.author | Mackay, Charles R. | |
dc.contributor.author | Sewell, William A. | |
dc.date.accessioned | 2017-05-03T16:02:16Z | |
dc.date.available | 2017-05-03T16:02:16Z | |
dc.date.issued | 2008 | |
dc.date.modified | 2011-09-15T05:46:24Z | |
dc.identifier.issn | 00221767 | |
dc.identifier.uri | http://hdl.handle.net/10072/38561 | |
dc.description.abstract | GM-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. | |
dc.description.peerreviewed | Yes | |
dc.description.publicationstatus | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | American Association of Immunologists | |
dc.publisher.place | United States | |
dc.publisher.uri | http://www.jimmunol.org/content/180/4/2600.short | |
dc.relation.ispartofstudentpublication | N | |
dc.relation.ispartofpagefrom | 2600 | |
dc.relation.ispartofpageto | 2607 | |
dc.relation.ispartofissue | 4 | |
dc.relation.ispartofjournal | Journal of Immunology | |
dc.relation.ispartofvolume | 180 | |
dc.rights.retention | Y | |
dc.subject.fieldofresearch | Allergy | |
dc.subject.fieldofresearch | Immunology | |
dc.subject.fieldofresearchcode | 110701 | |
dc.subject.fieldofresearchcode | 1107 | |
dc.title | Granulocyte-macrophage colony-stimulating factor is required for bronchial eosinophilia in a murine model of allergic airway inflammation | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dc.type.code | C - Journal Articles | |
gro.rights.copyright | Self-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. | |
gro.date.issued | 2008 | |
gro.hasfulltext | No Full Text | |
gro.griffith.author | Rolph, Michael S. | |