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* Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206; and
Wyeth Genetics Institute, Andover, MA 01810
The effectiveness of targeting IL-13 in models where airway
hyperresponsiveness (AHR) and airway inflammation have already been
established is not well-described. We investigated the effects of
blocking IL-13 on the early and late phase airway responses and the
development of AHR in previously sensitized and challenged mice.
BALB/cByJ mice were sensitized (days 1 and 14) and challenged (days
28–30) with OVA. Six weeks later (day 72), previously
sensitized/challenged mice were challenged with a single OVA aerosol
and the early and late phase response and development of AHR were
determined. Specific in vivo blockade of IL-13 was attained after i.p.
injection of a soluble IL-13R
2-IgG fusion protein (sIL-13R2Fc) on
days 71–72 for the early and late responses and on days 71–73 for the
development of AHR. sIL-13R2Fc administration inhibited the late,
but not early, phase response and the OVA challenge-induced changes in
lung resistance and dynamic compliance; as well, sIL-13R2Fc
administration decreased bronchoalveolar lavage eosinophilia and
mucus hypersecretion following the secondary challenge protocols. These
results demonstrate that targeting IL-13 alone regulates airway
responses when administrated to mice with established allergic airway
disease. These data identify the importance of IL-13 in the development
of allergen-induced altered airway responsiveness following airway
challenge, even when administered before rechallenge of mice in which
allergic disease had been previously
established.
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