Aspergillus fumigatus antigen exposure results in pulmonary airway resistance in wild-type but not in IL-4 knockout mice. Clin Immunol 1999 Mar;90(3):404-10
Date
03/17/1999Pubmed ID
10075870DOI
10.1006/clim.1998.4656Scopus ID
2-s2.0-0032953239 (requires institutional sign-in at Scopus site) 18 CitationsAbstract
Inhalation of Aspergillus fumigatus, a ubiquitous fungus, results in the development of allergic bronchopulmonary aspergillosis, a disabling allergic lung disease. For better patient management early diagnosis is essential, and understanding of the immune mechanism is important in achieving this goal. Although animal model studies have contributed to the understanding of the disease mechanism, details on the immunopathogenesis are still lacking. In the present study, we have developed an allergic aspergillosis model in wild-type and IL-4 knockout mice and studied the immune and airway responses. The results indicate that the immune response, pulmonary pathology, and airway reactivity comparable to allergic bronchopulmonary aspergillosis are reproducible in wild mice. IL-4 knockout mice showed similar pulmonary pathology, but no increase in airway resistance, suggesting that IgE and hence IL-4 may be important in eliciting the airway response, while other factors may be involved in the inflammatory process.
Author List
Kurup VP, Xia JQ, Rickaby DA, Dawson CA, Choi H, Fink JNMESH terms used to index this publication - Major topics in bold
Airway ResistanceAnimals
Antibodies, Fungal
Antibody Specificity
Antigens, Fungal
Aspergillosis, Allergic Bronchopulmonary
Aspergillus fumigatus
Eosinophils
Immunoglobulin E
Interleukin-4
Leukocyte Count
Lung
Methacholine Chloride
Mice
Mice, Inbred BALB C
Mice, Knockout
