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Am. J. Respir. Cell Mol. Biol., Volume 21, Number 4, October, 1999 480-489

Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness Requires Interleukin-5 but Not Immunoglobulin E or B Lymphocytes

Eckard Hamelmann, Katsuyuki Takeda, Jurgen Schwarze, Anthony T. Vella, Charles G. Irvin, and Erwin W. Gelfand

Division of Basic Sciences and Departments of Pediatrics and Medicine, National Jewish Medical and Research Center; and The Howard Hughes Medical Institute, Denver, Colorado

We previously defined a role for B cells and allergen-specific immunoglobulins in the development of allergic sensitization, airway inflammation, and airway hyperresponsiveness (AHR), using a 10-d protocol in which allergen exposure occurred exclusively via the airways, without adjuvant. In the present protocol, normal and B-cell-deficient (µMt-/-) mice were sensitized intraperitoneally to ovalbumin (OVA) and challenged with OVA via the airways in order to examine the requirements for AHR with this protocol. T-cell activation (antigen-specific proliferative responses and Th2-type cytokine production) and eosinophil infiltration in the peribronchial regions of the airways, with signs of eosinophil activation and degranulation, occurred in both experimental groups. In contrast to the 10-d protocol, increased in vivo airway responsiveness to methacholine and in vitro tracheal smooth-muscle responses to electrical field stimulation were observed in both normal and B-cell-deficient mice, and these responses were inhibited by anti-interleukin (IL)-5 administration before airway challenge. These data show that IL-5, but not B cells or allergen-specific IgE, are required for eosinophil airway infiltration and the development of AHR following allergen/alum sensitization and repeated airway challenge with allergen. These results emphasize that the use of different sensitization and challenge protocols can influence the requirements for development of AHR.




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