Background: Exposure to Aspergillus fumigatus allergens results in enhanced
total serum IgE and peripheral blood eosinophils in mice. The associated p
ulmonary inflammation and immunologic responses are comparable to those det
ected in human allergic bronchopulmonary aspergillosis. Allergen-induced cy
tokines are thought to regulate the inflammatory and immune responses in th
ese animals.
Methods: In the present study, we exposed C57BL/6 and BALB/c mice to A. fum
igatus antigen. Both wild-type and IL-4 knockout phenotypes of animals of b
oth strains were used. Some animals were also treated with anti-IL-5 or ant
i-IFN-gamma. Total serum IgE, Aspergillus species IgG subclass, peripheral
blood eosinophils, and lung histology were studied.
Results: The results demonstrate similar lung inflammation in all wild-type
and IL-4-/- animals exposed to A. fumigatus antigen. Similarly, in spite o
f the diverse immune response produced by the anticytokine treatment, no ma
jor differences were detected among any of the animal groups studied.
Conclusions: It can be concluded that A. fumigatus exposure in an immunolog
ically unaltered host is predominantly of a Th2 type, and that depletion of
the Th2 cytokine leads to a similar lung inflammation but with a character
istic Th1 response, suggesting that the pathogenesis of allergic aspergillo
sis is the result of multiple induction pathways.