Objective: Allergic bronchopulmonary aspergillosis, a disabling hypersensitivity lung disease, results from inhalation of Aspergillus fumigatus antigens present in contaminated environments. A murine model has been developed to understand the immune mechanism involved in allergic bronchopulmonary aspergillosis. We have investigated the immunoregulatory role of different physical forms of A. fumigatus antigens, such as A. fumigatus spores, soluble antigens, and soluble antigen coupled inert particles, in the model. Methods: BALB/c mice were exposed to soluble A. fumigatus antigens, spores, or inert particles of comparable size to the spores coupled with A. fumigatus soluble antigens. Antibody and eosinophil response, pulmonary pathology, and cytokine expressions were studied. Results: Peripheral blood eosinophilia and pulmonary inflammation with influx of eosinophils into the lung was detected more in animals exposed to particulate antigens than in those exposed to soluble antigen. However, the total serum IgE and Aspergillus-specificIgG levels showed only a slight increase in the former groups as opposed to elevated levels in animals exposed to soluble antigen. The cytokine expression in in vitro antigen stimulated spleen cells showed a typical Th2 pattern in all antigen-exposed animals. IL-5 mRNA could be detected in the spleen cells cultured with antigen from all groups of antigen-exposed animals. Conclusion: Particulate A. fumigatus antigens induced eosinophilia in mice prior to the elevation of serum IgE levels. This pattern of IgE and eosinophilia is reversed with the soluble antigen exposure in this model.
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