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* Division of Allergy, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
Pharmaceutical Research and Development, Johnson & Johnson, La Jolla, San Diego, CA 92130; and
Department of Dermatology, University of California, Davis, School of Medicine, Sacramento, CA 95817
We have studied murine models of asthma using
Fc
RI
-chain-deficient (FcRI-/-) mice to
investigate the role of IgE-dependent mast cell activation in these
models. When mice were either 1) immunized once with OVA in alum i.p.
and then challenged with OVA intranasally, or 2) repeatedly immunized
with OVA in the absence of adjuvant and subsequently challenged with
nebulized OVA, FcR-/- mice had significantly fewer
eosinophils and lower IL-4 levels in their bronchoalveolar lavage fluid
compared with wild-type mice. When mice were given anti-IL-5
antibody before OVA challenge in protocol 1, eosinophilic infiltration
into the airways was significantly suppressed in both genotypes, but
only FcRI-/- mice showed significantly reduced
airway hyperresponsiveness (AHR). In addition, when mice immunized and
challenged with OVA also received a late OVA provocation at a higher
concentration and were then exposed to methacholine, only wild-type
mice developed a substantial increase in AHR. Since FcRI is
expressed mainly on mast cells in mouse airways, we conclude that
IgE-dependent activation of this cell type plays an important role in
the development of allergic airway inflammation and AHR in mice. The
models used may be of value for testing inhibitors of IgE or mast cells
for development of therapeutic agents for human
asthma.
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