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*
Department of Immunology/Microbiology, Rush Medical College, Chicago, IL 60612; and
Department of Pediatrics, Cook County Children’s Hospital, Chicago, IL 60612
Neutrophil infiltration of the airways is a common finding in
respiratory syncytial virus (RSV) bronchiolitis. Neutrophil-derived
chemokines and neutrophil granule contents can cause further
inflammation, hyperresponsiveness, and damage of the airways. In this
study, peripheral blood neutrophils incubated with RSV (multiplicity of
infection (MOI) = 10) induced IL-8, macrophage inflammatory
protein (MIP)-1
, MIP-1ß, and myeloperoxidase (MPO) release. In
contrast, LPS induced only chemokine but not MPO release. RSV-induced
chemokine and MPO release was noncytotoxic as assessed by trypan blue
exclusion. The mechanism of RSV-induced chemokine release was shown to
be transcription dependent since cytokine mRNA synthesis was increased
with RSV stimulation and the process was inhibited by actinomycin-D. In
addition, the effect of dexamethasone (dex) on mediator release was
also studied. Dex significantly inhibited chemokine release but did not
inhibit MPO release. The mechanism of inhibition of the release of
these chemokines is probably posttranscriptional since the mRNA
synthesis was not inhibited by dex. We conclude that the release of
chemokines (IL-8, MIP-1, MIP-1ß) and granule enzymes (MPO) by
RSV-stimulated neutrophils may contribute to the pulmonary pathology in
RSV bronchiolitis. These in vitro findings showing that dex failed to
consistently inhibit all the RSV-induced release of neutrophil
inflammatory mediators may explain the variable efficacy of
corticosteroids in the treatment of RSV
bronchiolitis.
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