Induction of pulmonary allergen-specific IgA responses or airway hyperresponsiveness in the absence of allergic lung disease following sensitization with limiting doses of ovalbumin-alum

Cell Immunol. 2001 Sep 15;212(2):101-9. doi: 10.1006/cimm.2001.1854.

Abstract

Respiratory allergies represent a failure to generate nonpathogenic responses to innocuous foreign materials. Herein we assessed the role of the sensitizing dose of allergen in this response/nonresponse paradigm, sensitizing BALB/c mice with 5 ng-2 microg of OVA-alum and assessing their responses to repeated OVA aerosol challenge. Mice sensitized with < or = 25 ng of OVA-alum did not develop atopic antibodies, airway hyperresponsiveness (AHR), eosinophilia, or pulmonary Th2 responses, but the 25-ng group animals did develop significant IgA responses. The mice sensitized with 100 ng of OVA-alum developed AHR in the absence of detectable allergic disease, while the mice sensitized with 250 ng-2 microg of OVA/alum developed full-spectrum allergic disease (i.e., eosinophilia, IgE, IgG1, pulmonary Th2 cytokine responses, and AHR). These data indicate that limiting doses of allergen can differentially induce IgA or AHR in the absence of atopic disease in mice.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / immunology*
  • Alum Compounds / administration & dosage
  • Animals
  • Antibody Specificity
  • Bronchial Hyperreactivity / etiology*
  • Bronchial Hyperreactivity / immunology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Immunologic
  • Immunization
  • Immunoglobulin A / biosynthesis*
  • Immunoglobulin A / immunology
  • Immunoglobulin E / biosynthesis
  • Immunoglobulin E / genetics
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin G / genetics
  • Lung / immunology
  • Lung / pathology
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / administration & dosage
  • Ovalbumin / immunology*
  • Plethysmography, Whole Body
  • Pulmonary Eosinophilia / etiology
  • Pulmonary Eosinophilia / immunology
  • Respiratory Hypersensitivity / etiology*
  • Respiratory Hypersensitivity / immunology
  • Th2 Cells / immunology
  • Th2 Cells / metabolism

Substances

  • Allergens
  • Alum Compounds
  • Cytokines
  • Immunoglobulin A
  • Immunoglobulin G
  • ovalbumin-alum
  • Immunoglobulin E
  • Ovalbumin