Erythroid burst-promoting activity produced by interleukin-1-stimulated endothelial cells is granulocyte-macrophage colony-stimulating factor

G. M. Segal, E. McCall, G. C. Bagby

    Research output: Contribution to journalArticle

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    Abstract

    Interleukin-1 (IL-1) induces cultured human umbilical vein endothelial cells to elaborate heterogeneous hematopoietic growth factors, including granulocyte-macrophage and granulocyte colony-stimulating factors (GM-CSF and G-CSF, respectively). Because erythroid burst-promoting activity (BPA) is also elaborated by endothelial cells exposed to IL-1, we sought to determine whether the BPA released by IL-1-induced endothelial cells simply reflects the known erythropoietic activity of GM-CSF or whether other uncharacterized factors might be involved. Media conditioned by multiple passaged endothelial cells cultured for three days with recombinant IL-1α (ECM(IL-1)) stimulated erythroid burst and GM colony formation in cultures of human nonadherent T-lymphocyte-depleted marrow mononuclear cells. Pretreatment with an anti-GM-CSF antiserum neutralized all the BPA and 56% of the GM colony-stimulating activity (GM-CSA) in ECM(IL-1). The anti-serum used in these studies did not inhibit IL-3 or G-CSF activity and did not inhibit ECM-(IL-1)-induced murine GM colony growth (a measure of human G-CSF). To examine whether GM-CSF induces BPA release by accessory cells, media conditioned by marrow cells cultured for three days with GM-CSF were tested in the colony growth assays. Pretreatment with anti-GM-CSF antiserum completely neutralized the BPA and GM-CSA of the marrow cell-conditioned medium. We conclude that GM-CSF is the BPA elaborated by IL-1-induced endothelial cells. The in vitro erythropoietic activity of GM-CSF is not dependent on induced BPA release by accessory cells and therefore likely results from a direct effect of GM-CSF on progenitor cells.

    Original languageEnglish (US)
    Pages (from-to)1364-1367
    Number of pages4
    JournalBlood
    Volume72
    Issue number4
    StatePublished - 1988

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    Endothelial cells
    Granulocyte-Macrophage Colony-Stimulating Factor
    Interleukin-1
    Endothelial Cells
    Military electronic countermeasures
    Granulocyte Colony-Stimulating Factor
    Conditioned Culture Medium
    Bone Marrow
    Accessories
    Immune Sera
    Cells
    T-cells
    Interleukin-3
    Human Umbilical Vein Endothelial Cells
    Growth
    Cell culture
    Granulocytes
    Cultured Cells
    Assays
    Intercellular Signaling Peptides and Proteins

    ASJC Scopus subject areas

    • Hematology

    Cite this

    Erythroid burst-promoting activity produced by interleukin-1-stimulated endothelial cells is granulocyte-macrophage colony-stimulating factor. / Segal, G. M.; McCall, E.; Bagby, G. C.

    In: Blood, Vol. 72, No. 4, 1988, p. 1364-1367.

    Research output: Contribution to journalArticle

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    abstract = "Interleukin-1 (IL-1) induces cultured human umbilical vein endothelial cells to elaborate heterogeneous hematopoietic growth factors, including granulocyte-macrophage and granulocyte colony-stimulating factors (GM-CSF and G-CSF, respectively). Because erythroid burst-promoting activity (BPA) is also elaborated by endothelial cells exposed to IL-1, we sought to determine whether the BPA released by IL-1-induced endothelial cells simply reflects the known erythropoietic activity of GM-CSF or whether other uncharacterized factors might be involved. Media conditioned by multiple passaged endothelial cells cultured for three days with recombinant IL-1α (ECM(IL-1)) stimulated erythroid burst and GM colony formation in cultures of human nonadherent T-lymphocyte-depleted marrow mononuclear cells. Pretreatment with an anti-GM-CSF antiserum neutralized all the BPA and 56{\%} of the GM colony-stimulating activity (GM-CSA) in ECM(IL-1). The anti-serum used in these studies did not inhibit IL-3 or G-CSF activity and did not inhibit ECM-(IL-1)-induced murine GM colony growth (a measure of human G-CSF). To examine whether GM-CSF induces BPA release by accessory cells, media conditioned by marrow cells cultured for three days with GM-CSF were tested in the colony growth assays. Pretreatment with anti-GM-CSF antiserum completely neutralized the BPA and GM-CSA of the marrow cell-conditioned medium. We conclude that GM-CSF is the BPA elaborated by IL-1-induced endothelial cells. The in vitro erythropoietic activity of GM-CSF is not dependent on induced BPA release by accessory cells and therefore likely results from a direct effect of GM-CSF on progenitor cells.",
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    N2 - Interleukin-1 (IL-1) induces cultured human umbilical vein endothelial cells to elaborate heterogeneous hematopoietic growth factors, including granulocyte-macrophage and granulocyte colony-stimulating factors (GM-CSF and G-CSF, respectively). Because erythroid burst-promoting activity (BPA) is also elaborated by endothelial cells exposed to IL-1, we sought to determine whether the BPA released by IL-1-induced endothelial cells simply reflects the known erythropoietic activity of GM-CSF or whether other uncharacterized factors might be involved. Media conditioned by multiple passaged endothelial cells cultured for three days with recombinant IL-1α (ECM(IL-1)) stimulated erythroid burst and GM colony formation in cultures of human nonadherent T-lymphocyte-depleted marrow mononuclear cells. Pretreatment with an anti-GM-CSF antiserum neutralized all the BPA and 56% of the GM colony-stimulating activity (GM-CSA) in ECM(IL-1). The anti-serum used in these studies did not inhibit IL-3 or G-CSF activity and did not inhibit ECM-(IL-1)-induced murine GM colony growth (a measure of human G-CSF). To examine whether GM-CSF induces BPA release by accessory cells, media conditioned by marrow cells cultured for three days with GM-CSF were tested in the colony growth assays. Pretreatment with anti-GM-CSF antiserum completely neutralized the BPA and GM-CSA of the marrow cell-conditioned medium. We conclude that GM-CSF is the BPA elaborated by IL-1-induced endothelial cells. The in vitro erythropoietic activity of GM-CSF is not dependent on induced BPA release by accessory cells and therefore likely results from a direct effect of GM-CSF on progenitor cells.

    AB - Interleukin-1 (IL-1) induces cultured human umbilical vein endothelial cells to elaborate heterogeneous hematopoietic growth factors, including granulocyte-macrophage and granulocyte colony-stimulating factors (GM-CSF and G-CSF, respectively). Because erythroid burst-promoting activity (BPA) is also elaborated by endothelial cells exposed to IL-1, we sought to determine whether the BPA released by IL-1-induced endothelial cells simply reflects the known erythropoietic activity of GM-CSF or whether other uncharacterized factors might be involved. Media conditioned by multiple passaged endothelial cells cultured for three days with recombinant IL-1α (ECM(IL-1)) stimulated erythroid burst and GM colony formation in cultures of human nonadherent T-lymphocyte-depleted marrow mononuclear cells. Pretreatment with an anti-GM-CSF antiserum neutralized all the BPA and 56% of the GM colony-stimulating activity (GM-CSA) in ECM(IL-1). The anti-serum used in these studies did not inhibit IL-3 or G-CSF activity and did not inhibit ECM-(IL-1)-induced murine GM colony growth (a measure of human G-CSF). To examine whether GM-CSF induces BPA release by accessory cells, media conditioned by marrow cells cultured for three days with GM-CSF were tested in the colony growth assays. Pretreatment with anti-GM-CSF antiserum completely neutralized the BPA and GM-CSA of the marrow cell-conditioned medium. We conclude that GM-CSF is the BPA elaborated by IL-1-induced endothelial cells. The in vitro erythropoietic activity of GM-CSF is not dependent on induced BPA release by accessory cells and therefore likely results from a direct effect of GM-CSF on progenitor cells.

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