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Departments of
*
Medicine,
Molecular Virology, and
Pediatrics, University of Wisconsin, Madison, WI 53792
Episodes of virus-induced exacerbations of asthma are accompanied
by increased eosinophils (EOS) in respiratory secretions and evidence
of EOS degranulation. Although rhinoviruses (RV) are the viruses most
often implicated in exacerbations of asthma in both children and
adults, little is known about the immune response to this group of
viruses and, in particular, EOS-RV interactions. To define such
interactions, we incubated human rhinovirus type 16 (RV16), a serotype
using ICAM-1 as a receptor, with EOS purified from PBMC, and measured
EOS-RV binding, EOS-mediated Ag presentation and T cell activation, and
EOS cell surface marker expression and superoxide production.
Significant RV16 binding occurred to EOS that were pretreated with
granulocyte-macrophage CSF, and this binding was inhibited by
anti-ICAM-1 mAb. EOS also presented viral Ags to RV16-specific T
cells, causing T cell proliferation and secretion of IFN-
. RV16
induced a significant shift from CD18dim to
CD18bright, but did not affect EOS expression of CD54,
CD69, or HLA-DR. Finally, RV16 did not induce superoxide production
from peripheral blood EOS. These findings suggest that RV16 also binds
to airway EOS, which resemble granulocyte-macrophage CSF-treated blood
EOS in terms of high expression of ICAM-1. Furthermore, our findings
suggest that EOS could participate in RV-induced immune responses
through Ag presentation and T cell activation. By activating
RV-specific T cells, EOS may play an important role in the initiation
of antiviral T cell responses, and these effects could also contribute
to enhanced airway inflammation and increased asthma symptoms in
susceptible individuals.
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