Granulocyte-macrophage colony-stimulating factor is required for bronchial eosinophilia in a murine model of allergic airway inflammation

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Title Granulocyte-macrophage colony-stimulating factor is required for bronchial eosinophilia in a murine model of allergic airway inflammation
Author Su, Yung-Chang; Rolph, Michael; Hansbro, Nicole G.; Mackay, Charles R.; Sewell, William A.
Journal Name Journal of Immunology
Year Published 2008
Place of publication United States
Publisher American Association of Immunologists
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-γ mRNA and protein were increased in the lung tissue and BAL fluid in GM-CSF–/– mice, as were mRNA levels of the IFN-γ-inducible chemokines CXCL9 (Mig), CXCL10 (IP-10), and CXCL11 (I-Tac). Interestingly, these IFN-γ-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.
Peer Reviewed Yes
Published Yes
Publisher URI http://www.jimmunol.org/content/180/4/2600.short
Copyright Statement 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.
Volume 180
Issue Number 4
Page from 2600
Page to 2607
ISSN 0022-1767
Date Accessioned 2011-03-16
Date Available 2011-09-15T05:46:24Z
Language en_AU
Faculty Faculty of Science, Environment, Engineering and Technology
Subject Allergy
URI http://hdl.handle.net/10072/38561
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1x

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