The Journal of Experimental Medicine
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Published 7 January 2002. doi:10.1084/jem.20011732
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© Rockefeller University Press, 0022-1007/2002/1/51/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 1, January 7, 2002 51-57

Original Article

The Absence of Interleukin 9 Does Not Affect the Development of Allergen-induced Pulmonary Inflammation nor Airway Hyperreactivity

Sarah J. McMillan1, Benjamin Bishop1, Michael J. Townsend2, Andrew N. McKenzie2 and Clare M. Lloyd1

1 Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England
2 Medical Research Council Laboratory for Molecular Biology, Cambridge CB2 2QH, England

Address correspondence to Clare M. Lloyd, Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England. Phone: 44-207-594-3102; Fax: 44-207-594-3119; E-mail: c.lloyd{at}ic.ac.uk

Interleukin (IL)-9 is a pleiotropic cytokine secreted by T helper (Th)2 cells and has been proposed as a candidate gene for asthma and allergy. We have used mice genetically deficient in IL-9 to determine the role of this cytokine in the pathophysiologic features of the allergic pulmonary response–airway hyperreactivity (AHR) and eosinophilia. We have demonstrated that IL-9 is not required for the development of a robust Th2 response to allergen in sensitized mice. IL-9 knockout mice developed a similar degree of eosinophilic inflammation and AHR to their wild-type littermates. Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9. Moreover, levels of bronchoalveolar lavage (BAL) IL-4, IL-5, and IL-13 were comparable between wild-type and knockout mice. These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion.

Key Words: Th2 cytokines • asthma • airway hyperreactivity • eosinophilia • mucus


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