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Viral Immunology Laboratory, Centre de Recherche en Rhumatologie et Immunologie, Centre de Recherche du Centre Hospitalier de l’Université Laval, Québec, Canada; and
Molecular Inflammation Laboratory, Department of Microbiology & Immunology, The University of Adelaide, Adelaide, South Australia
We have recently demonstrated that EBV binds to human neutrophils
and stimulates a wide range of activities, including homeotypic
aggregation, total RNA synthesis, and expression of the chemokines IL-8
and macrophage inflammatory protein-1
(MIP-1). Neutrophil
function is also known to be modulated by priming with
granulocyte-macrophage colony-stimulating factor (GM-CSF). We have
therefore investigated the modulation of EBV-induced activation of
human neutrophils by GM-CSF. Treatment of neutrophils with GM-CSF
before EBV activation enhanced the production of both MIP-1 and
IL-8. The IL-8 produced under these conditions was biologically active
as determined in the calcium mobilization assay. GM-CSF was also found
to increase the ability of EBV to prime neutrophils for increased
leukotriene B4 (LTB4) synthesis. Prior
treatment of GM-CSF with neutralizing Abs inhibited these effects.
GM-CSF also increased the specific binding of FITC-EBV to the
neutrophil surface, as evaluated by fluorocytometry. Local production
of GM-CSF in tissues invaded by EBV could therefore serve to potentiate
a host defense mechanism directed toward the destruction of the
infectious virus via increased production of chemotactic factors. Since
both IL-8 and MIP-1 are reported to be chemoattractants in vitro for
T cells and T and B cells, respectively, the ability of EBV to induce
their production by neutrophils may enhance its ability to infect B and
T lymphocytes via increased recruitment to sites of infection.
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