Roberge, C.McColl, S.Larochelle, B.Gosselin, J.2006-07-052006-07-051998Journal of Immunology, 1998; 160(5):2442-24480022-17671550-6606http://hdl.handle.net/2440/11627We 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-1alpha (MIP-1alpha). 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-1alpha 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-1alpha 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.enNeutrophilsHumansHerpesvirus 4, HumanCalciumLeukotriene B4Granulocyte-Macrophage Colony-Stimulating FactorRNA, MessengerInterleukin-8Macrophage Inflammatory ProteinsChemotactic FactorsAdjuvants, ImmunologicNeutrophil ActivationChemokine CCL3Chemokine CCL4Journal article0030004193001998222510.4049/jimmunol.160.5.24420000721157000522-s2.0-003203226368199McColl, S. [0000-0003-0949-4660]