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Published ahead of print on December 30, 2003, doi:10.1164/rccm.200305-706OC

Am. J. Respir. Crit. Care Med., Volume 169, Number 7, April 2004, 860-867

A more recent version of this article appeared on April 1, 2004
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Submitted on May 28, 2003
Accepted on December 28, 2003

Type 2 Cytokines in the Pathogenesis of Sustained Airway Dysfunction and Airway Remodeling in Mice

Richard Leigh, Russ Ellis, Jennifer N Wattie, Jeremy A Hirota, Klaus I Matthaei, Paul S Foster, Paul M O'Byrne, and Mark D Inman*

* To whom correspondence should be addressed. E-mail: inmanma{at}mcmaster.ca.

The mechanisms underlying airway hyperresponsiveness remain unclear, although airway inflammation and remodeling likely play important roles. We have observed sustained airway hyperreactivity and airway remodeling occurring in mice following chronic allergen exposure, and persisting beyond resolution of allergen-induced inflammation. The aim of this study was to delineate mechanisms involved in allergen-induced airway hyperreactivity and airway remodeling, and to examine evidence for a causal association between airway remodeling and sustained airway hyperreactivity. Wild-type and interleukin-4, interleukin-5 and interleukin-13 deficient (-/-) mice were sensitized and studied 4 weeks after chronic allergen exposure. By measuring airway responsiveness and airway morphometry, we demonstrated that wild-type mice developed sustained airway hyperreactivity and aspects of airway remodeling following chronic allergen exposure. Both interleukin-4-/- and interleukin-13-/- mice were protected from developing sustained airway hyperreactivity and aspects of airway remodeling. In contrast, interleukin-5-/- mice developed sustained airway hyperreactivity and aspects of airway remodeling similar to that seen in wild type mice. Our results confirm that interleukin-4 and interleukin-13, but not interleukin-5, are critical for the development of sustained airway hyperreactivity and airway remodeling following allergen exposure.
Key words: Allergic disease, asthma, bronchial hyperreactivity, IL-4, IL-5, IL-13




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