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J. Exp. Med.,
Volume 188, Number 7, October 5, 1998 1307-1320
By
From the * Section of Immunobiology and 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.
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
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