Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleukin-5 but not immunoglobulin E or B lymphocytes

Am J Respir Cell Mol Biol. 1999 Oct;21(4):480-9. doi: 10.1165/ajrcmb.21.4.3659.


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 (microMt(-/-)) 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Allergens / administration & dosage
  • Animals
  • Asthma / etiology
  • Asthma / immunology
  • B-Lymphocytes / immunology
  • Bronchial Hyperreactivity / etiology*
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / pathology
  • Cytokines / biosynthesis
  • Disease Models, Animal
  • Eosinophilia / etiology*
  • Eosinophilia / immunology
  • Eosinophilia / pathology
  • Female
  • Humans
  • Immunoglobulin E / metabolism
  • Interleukin-5 / antagonists & inhibitors
  • Interleukin-5 / immunology
  • Interleukin-5 / pharmacology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Ovalbumin / immunology
  • T-Lymphocytes / immunology


  • Allergens
  • Cytokines
  • Interleukin-5
  • Immunoglobulin E
  • Ovalbumin