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Am. J. Respir. Cell Mol. Biol., Volume 19, Number 5, November, 1998 713-720

RAPID COMMUNICATION
Interleukin-9 Promotes Allergen-Induced Eosinophilic Inflammation and Airway Hyperresponsiveness in Transgenic Mice

Michael P. McLane, Angela Haczku, Matthijs van de Rijn, Christine Weiss, Veronica Ferrante, Dorothy MacDonald, Jean-Christophe Renauld, Nicholas C. Nicolaides, Kenneth J. Holroyd, and Roy C. Levitt

Magainin Institute of Molecular Medicine, Magainin Pharmaceuticals, Plymouth Meeting; Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania; and The Ludwig Institute for Cancer Research and Experimental Medicine Unit, University of Louvain, Brussels, Belgium

Human atopic asthma is a complex heritable inflammatory disorder of the airways associated with clinical signs of allergic inflammation and airway hyperresponsiveness. Recent studies demonstrate that the degree of airway responsiveness is strongly associated with interleukin (IL)-9 expression in murine lung. To investigate the contribution of IL-9 to airway hyperresponsiveness, and to explore directly its relationship to airway inflammation, we studied transgenic mice overexpressing IL-9. In this report we show that IL-9 transgenic mice (FVB/N-TG5), in comparison with FVB/NJ mice, display significantly enhanced eosinophilic airway inflammation, elevated serum total immunoglobulin E, and airway hyperresponsiveness following lung challenge with a natural antigen (Aspergillus fumigatus). These data support a central role for IL-9 in the complex pathogenesis of allergic inflammation.




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