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B in Airway Epithelium in a Murine Model of Allergic Airway Inflammation
From the Vermont Lung Center and Departments ofPathology* and Medicine,University of Vermont, Burlington, Vermont
Bronchiolar epithelium is postulated to play a critical role in the
orchestration of responses to inhaled allergens, and may
contribute to the pathogenesis of asthma. Using a murine model of
allergic airway inflammation and hyperresponsiveness, we
demonstrate in mice sensitized with ovalbumin (OVA) that following a
single challenge with nebulized OVA, a rapid and protracted
activation of inhibitor of kappa B kinase (IKK) occurred in lung
tissue. IKK activation was followed by nuclear localization of nuclear
factor (NF)-
B within the bronchiolar epithelium and increased
luciferase activity in lungs of mice containing a NF-B-dependent
reporter gene. Challenge of sensitized mice with OVA also induced mRNA
expression of the chemokines, macrophage inflammatory protein-2
(MIP-2) and eotaxin in lung tissue, which corresponded
temporally with the observed influx of neutrophils and
eosinophils, respectively, into the airspaces. Using
laser capture microdissection and quantitative polymerase chain
reaction, we demonstrated that MIP-2 and eotaxin were
predominantly expressed in bronchiolar epithelium, in contrast
to distal regions of the lungs, which expressed lower or
undetectable levels of these mRNAs. These studies strengthen the
potential importance of the bronchiolar epithelial cell as a source of
production of NF-B-dependent mediators that play a role in
asthma.
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