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*
Division of Allergy, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121; and
Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037
IgE is present in airway secretions from human patients with
allergic rhinitis and bronchial asthma. However, the contribution of
IgE present locally to the overall airway inflammation is not well
understood. We hypothesize that Ag-specific IgE can capture airborne
Ags and form immune complexes. These immune complexes may function as
potent inducers of immune responses in the lung, contributing to the
perpetuation of airway inflammation. BALB/c mice were first sensitized
with OVA in alum systemically and then challenged with nebulized OVA.
Bronchoalveolar lavage (BAL) fluid from these mice contained
significant amounts of IgE, of which >50% was Ag specific. The IgE
levels in airway secretions remained elevated for more than 15 days
after the termination of Ag exposure. Significant amounts of IgE-OVA
immune complexes were detected in BAL fluid from the OVA-challenged
mice. For comparison of IgE immune complexes vs Ag alone, we treated
OVA-immunized mice with intranasal administration of trinitrophenyl-OVA
or trinitrophenyl-OVA-anti-DNP IgE. Those treated with the immune
complexes showed significantly higher levels of IL-4 and more
pronounced eosinophilia in BAL fluid than did those receiving the Ag
alone. The IgE immune complexes did not augment the inflammatory
response in high affinity IgE receptor (Fc
RI)-deficient mice. We
conclude that IgE present in the airways can capture the Ag and that
the immune complexes thus formed may augment allergic airway response
in an FcRI-dependent manner. Thus, IgE present in airway secretions
may facilitate Ag-mediated allergic airway
inflammation.
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