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-Inducing Factor (IL-18) Increases Allergic Sensitization, Serum IgE, Th2 Cytokines, and Airway Eosinophilia in a Mouse Model of Allergic Asthma1
*
Department of Internal Medicine, Division of Allergy and Immunology, University of Texas Medical Branch, Galveston, TX 77555;
Department of Medicine, East Carolina University School of Medicine, Greenville, NC; and
Fujisaki Institute, Hayashibara Biochemical Labs, Okayama, Japan
We investigated the effects of IFN-
-inducing factor (IL-18) in a
ragweed (RW) mouse model of allergic asthma. Administration of IL-18 in
conjunction with allergic sensitization and challenge in wild-type, but
not IFN- -/- mice, inhibited the bronchoalveolar
lavage (BAL) eosinophilia induced by RW challenge, and increased serum
levels of RW-specific IgG2a and production of IFN- from splenocytes
cultured with RW, indicating a critical role for IFN- in mediating
these effects. Paradoxically, the same treatment schedule in WT mice
increased serum levels of RW-specific IgE and IgG1, and
production of IL-4 and IL-5 from splenocytes cultured with RW. When the
effects of the same IL-18 treatment schedule were allowed to mature for
3 wk, the inhibition of lung eosinophil recruitment was replaced by
augmentation of lung eosinophil recruitment. In another experiment,
IL-18 administered only with allergic sensitization increased BAL
eosinophilia and lung expression of IL-5 and IFN-, while IL-18
administered only with RW challenge decreased BAL eosinophilia and
increased lung IFN- expression, while lung expression of IL-5
remained unchanged. IL-18 administered without RW or adjuvant to naive
mice increased total serum IgE levels. Finally, intrapulmonary
administrations of IL-18 plus RW in naive mice dramatically increased
Th2 cytokine production, IgE levels, eosinophil recruitment, and airway
mucus, demonstrating induction of allergic sensitization. This is the
first report demonstrating that IL-18 promotes a Th2 phenotype in vivo,
and potently induces allergic sensitization. These results suggest that
IL-18 may contribute to the pathogenesis of allergic
asthma.
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