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B Activity in the Bronchi of an Animal Model of Asthma1
Departments of
*
Physiology and
Immunology/Vaccinology, Faculty of Veterinary Medicine, and
Laboratory of Medical Chemistry/Medical Oncology, Faculty of Medicine, University of Liege, Liege, Belgium
In most cells trans-activating NF-
B induces many
inflammatory proteins as well as its own inhibitor, IB-
, thus
assuring a transient response upon stimulation. However,
NF-B-dependent inflammatory gene expression is persistent in
asthmatic bronchi, even after allergen eviction. In the present report
we used bronchial brushing samples (BBSs) from heaves-affected horses
(a spontaneous model of asthma) to elucidate the mechanisms by which
NF-B activity is maintained in asthmatic airways. NF-B activity
was high in granulocytic and nongranulocytic BBS cells. However,
NF-B activity highly correlated to granulocyte percentage and was
only abrogated after granulocytic death in cultured BBSs. Before
granulocytic death, NF-B activity was suppressed by simultaneous
addition of neutralizing anti-IL-1
and anti-TNF- Abs to
the medium of cultured BBSs. Surprisingly, IB-, whose expression
is not regulated by NF-B, unlike IB-, was the most prominent
NF-B inhibitor found in BBSs. The amounts of IB- were low in
BBSs obtained from diseased horses, but drastically increased after
addition of the neutralizing anti-IL-1 and anti-TNF- Abs.
These results indicate that sustained NF-B activation in asthmatic
bronchi is driven by granulocytes and is mediated by IL-1 and
TNF-. Moreover, an imbalance between high levels of IL-1- and
TNF--mediated IB- degradation and low levels of IB-
synthesis is likely to be the mechanism preventing NF-B deactivation
in asthmatic airways before granulocytic death.
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