The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/10/1307/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 7, October 5, 1998 1307-1320

Articles

Expression of Interleukin 9 in the Lungs of Transgenic Mice Causes Airway Inflammation, Mast Cell Hyperplasia, and Bronchial Hyperresponsiveness

Ulla-Angela Temann*, Gregory P. Geba{ddagger}, John A. Rankin§, and Richard A. Flavell*,||

From the * Section of Immunobiology and {ddagger} Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520; § Pulmonary and Critical Care Medicine, Veteran's Administration Connecticut Health Care System, West Haven, Connecticut 06516; and the || Howard Hughes Medical Institute, New Haven, Connecticut 06520

Interleukin (IL)-9, a pleiotropic cytokine produced by the Th2 subset of T lymphocytes has been proposed as product of a candidate gene responsible for asthma. Its wide range of biological functions on many cell types involved in the allergic immune response suggests a potentially important role in the complex pathogenesis of asthma. To investigate the contributions of IL-9 to airway inflammation and airway hyperresponsiveness in vivo, we created transgenic mice in which expression of the murine IL-9 cDNA was regulated by the rat Clara cell 10 protein promoter. Lung selective expression of IL-9 caused massive airway inflammation with eosinophils and lymphocytes as predominant infiltrating cell types. A striking finding was the presence of increased numbers of mast cells within the airway epithelium of IL-9–expressing mice. Other impressive pathologic changes in the airways were epithelial cell hypertrophy associated with accumulation of mucus-like material within nonciliated cells and increased subepithelial deposition of collagen. Physiologic evaluation of IL-9–expressing mice demonstrated normal baseline airway resistance and markedly increased airway hyperresponsiveness to inhaled methacholine. These findings strongly support an important role for IL-9 in the pathogenesis of asthma.

Key Words: interleukin 9 • transgenic mice • asthma • mast cells • eosinophilia

Address correspondence to Richard A. Flavell, Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520. Phone: 203-737-2216; Fax: 203-785-7561; E-mail: richard.flavell{at}qm.yale.edu


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