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Published ahead of print on July 8, 2004, doi:10.1164/rccm.200311-1488OC
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American Journal of Respiratory and Critical Care Medicine Vol 170. pp. 851-856, (2004)
© 2004 American Thoracic Society
doi: 10.1164/rccm.200311-1488OC

Is Interleukin-13 Critical in Maintaining Airway Hyperresposiveness in Allergen-challenged Mice?

Richard Leigh, Russ Ellis, Jennifer Wattie, Debra D. Donaldson and Mark D. Inman

Firestone Institute for Respiratory Health, St. Joseph's Healthcare, McMaster University, Hamilton, Ontario, Canada; and Wyeth Research, Wyeth Pharmaceuticals Inc., Cambridge, MA

Correspondence and requests for reprints should be addressed to Mark D. Inman, M.D., Ph.D., Firestone Institute for Respiratory Health, St. Joseph's Healthcare, 50 Charlton Avenue East, Hamilton, ON, L8N 4A6 Canada. E-mail: inmanma{at}mcmaster.ca

Interleukin (IL)-13 is regarded as being a central effector in the pathophysiology of airway hyperresponsiveness. We have described a mouse model in which chronic allergen exposure results in sustained airway hyperresponsiveness and aspects of airway remodeling, and here sought to demonstrate that this component of airway hyperresponsiveness is independent of biologically active IL-13. Sensitized mice were subjected to either brief or chronic periods of allergen exposure and studied 24 hours after brief or 4 weeks after chronic allergen inhalation. A soluble murine anti–IL-13 receptor fusion protein that specifically binds to and neutralizes IL-13 was given daily during the 4 days before the day of outcome measurements in both protocols. Outcome measurements included airway responses to intravenous methacholine, bronchoalveolar lavage fluid cell counts, and airway morphometry. Compared with the saline control, brief allergen challenge resulted in airway hyperresponsiveness, which was prevented by anti–IL-13 treatment. Chronic allergen challenge resulted in sustained airway hyperresponsiveness and indices of airway remodeling; IL-13 blockade failed to reverse this sustained airway hyperresponsiveness. These results confirm that IL-13 is critical for the development of airway hyperresponsiveness associated with brief allergen exposure, but is not necessary to maintain the sustained airway hyperresponsiveness associated with airway remodeling.

Key Words: airway inflammation • allergic disease • asthma • bronchial hyperreactivity




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