Maintenance of airway hyperresponsiveness in chronic asthma may be mediated by Th2-independent mechanisms9734;

N.J. Lina, J.R. Baker Jra, J.M. Schuhb, C.M. Hogaboamb

Author address: 

a Division of Allergy and Immunology, University of Michigan, Ann Arbor, MI, USA b Department of Pathology, University of Michigan, Ann Arbor, MI, USA


Rationale CD4+, Th2-mediated inflammation is an important component of airway hyperresponsiveness (AHR) in allergic airway disease. IL-4 and IL-13, the prototypic Th2 cytokines, mediate their effects through a common receptor complex made up of IL-4Rα and IL-13Rα 1. In this study, we examined the effects of impaired Th2 signaling on AHR using IL-4Rα 8722;/8722; mice in a murine model of allergic asthma. Methods IL-4Rα 8722;/8722; mice and control BALB/c (IL-4Rα +/+) mice were sensitized to and challenged with Aspergillus fumigatus. Airway disease was assessed at days 14, 28, 51, and 57 after intratracheal conidia challenge. AHR was evaluated by plethysmography after intravenous methacholine. Whole lung levels of cytokines, chemokines, and immunoglobulins were measured by specific ELISA. Paraffin-embedded lung sections were stained for histology. Bronchoalveolar lavage (BAL) fluid was cytospun for differential cell counts. Results While AHR was significantly reduced in IL-4Rα 8722;/8722; mice (p

abstract No: 

Page S173

Full conference title: 

2004 American Academy of Allergy, Asthma, and Immunology Annual Meeting
    • AAAAI 2004 (60th)