Macrophage inflammatory protein (MIP)-1β abrogates the capacity of MIP-1α to suppress myeloid progenitor cell growth

H. E. Broxmeyer, B. Sherry, S. Cooper, F. W. Ruscetti, D. E. Williams, P. Arosio, B. S. Kwon, A. Cerami

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Abstract

The effects of recombinant murine macrophage inflammatory protein (MIP)-1β and MIP-2 on the suppressive activity of MIP-1α were tested using colony formation by human and murine bone marrow burst-forming unit-erythroid (BFU-E), colony-forming unit-granulocyte erythroid macrophage, megakaryocyte (CFU-GEMM), and colony-forming unit-granulocyte macrophage (CFU-GM) progenitor cells. MIP-1β, but not MIP-2, when added with MIP-1α to cells, blocked the suppressive effects of MIP-1α on both human and murine BFU-E, CFU-GEMM, and CFU-GM colony formation. Similar results were observed regardless of the early acting cytokines used: human rGM-CSF plus human rIL-3, and two recently described potent cytokines, a genetically engineered human rGM-CSF/IL-3 fusion protein and MGF, a c-kit ligand. The more potent the stimuli, the greater the suppressive activity noted. Pulse treatment of hu bone marrow cells with MIP-1α at 4°C for 1 h was as effective in inhibiting colony formation as continuous exposure of cells to MIP-1α, and the pulsing effect with MIP-1α could not be overcome by subsequent exposure of cells to MIP-1β. Also, pulse exposure of cells to MIP-1β blocked the activity of subsequently added MIP-1α. For specificity, the action of a nonrelated myelosuppressive factor H-ferritin, was compared. MIP-1α and H-ferritin were shown to act on similar target populations of early BFU-E, CFU-GEMM, and CFU-GM. MIP-1β did not block the suppressive activity of H-ferritin. Also, hemin and an inactive recombinant human H-ferritin mutein counteracted the suppressive effects of the wildtype H-ferritin molecule, but did not block the suppressive effects of MIP-1α. These results show that MIP-1β's ability to block the action of MIP-1α is specific. In addition, the results suggest that MIP-1α and MIP-β can, through rapid action, modulate early myeloid progenitor cell proliferation.

Original languageEnglish (US)
Pages (from-to)2586-2594
Number of pages9
JournalJournal of Immunology
Volume147
Issue number8
StatePublished - Nov 8 1991

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Myeloid Progenitor Cells
Macrophage Inflammatory Proteins
Growth
Apoferritins
Erythroid Precursor Cells
Chemokine CXCL2
Granulocytes
Macrophages
Cytokines
Complement Factor H
Hemin
Granulocyte-Macrophage Progenitor Cells
Stem Cell Factor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Broxmeyer, H. E., Sherry, B., Cooper, S., Ruscetti, F. W., Williams, D. E., Arosio, P., ... Cerami, A. (1991). Macrophage inflammatory protein (MIP)-1β abrogates the capacity of MIP-1α to suppress myeloid progenitor cell growth. Journal of Immunology, 147(8), 2586-2594.

Macrophage inflammatory protein (MIP)-1β abrogates the capacity of MIP-1α to suppress myeloid progenitor cell growth. / Broxmeyer, H. E.; Sherry, B.; Cooper, S.; Ruscetti, F. W.; Williams, D. E.; Arosio, P.; Kwon, B. S.; Cerami, A.

In: Journal of Immunology, Vol. 147, No. 8, 08.11.1991, p. 2586-2594.

Research output: Contribution to journalArticle

Broxmeyer, HE, Sherry, B, Cooper, S, Ruscetti, FW, Williams, DE, Arosio, P, Kwon, BS & Cerami, A 1991, 'Macrophage inflammatory protein (MIP)-1β abrogates the capacity of MIP-1α to suppress myeloid progenitor cell growth', Journal of Immunology, vol. 147, no. 8, pp. 2586-2594.
Broxmeyer, H. E. ; Sherry, B. ; Cooper, S. ; Ruscetti, F. W. ; Williams, D. E. ; Arosio, P. ; Kwon, B. S. ; Cerami, A. / Macrophage inflammatory protein (MIP)-1β abrogates the capacity of MIP-1α to suppress myeloid progenitor cell growth. In: Journal of Immunology. 1991 ; Vol. 147, No. 8. pp. 2586-2594.
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AU - Ruscetti, F. W.

AU - Williams, D. E.

AU - Arosio, P.

AU - Kwon, B. S.

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N2 - The effects of recombinant murine macrophage inflammatory protein (MIP)-1β and MIP-2 on the suppressive activity of MIP-1α were tested using colony formation by human and murine bone marrow burst-forming unit-erythroid (BFU-E), colony-forming unit-granulocyte erythroid macrophage, megakaryocyte (CFU-GEMM), and colony-forming unit-granulocyte macrophage (CFU-GM) progenitor cells. MIP-1β, but not MIP-2, when added with MIP-1α to cells, blocked the suppressive effects of MIP-1α on both human and murine BFU-E, CFU-GEMM, and CFU-GM colony formation. Similar results were observed regardless of the early acting cytokines used: human rGM-CSF plus human rIL-3, and two recently described potent cytokines, a genetically engineered human rGM-CSF/IL-3 fusion protein and MGF, a c-kit ligand. The more potent the stimuli, the greater the suppressive activity noted. Pulse treatment of hu bone marrow cells with MIP-1α at 4°C for 1 h was as effective in inhibiting colony formation as continuous exposure of cells to MIP-1α, and the pulsing effect with MIP-1α could not be overcome by subsequent exposure of cells to MIP-1β. Also, pulse exposure of cells to MIP-1β blocked the activity of subsequently added MIP-1α. For specificity, the action of a nonrelated myelosuppressive factor H-ferritin, was compared. MIP-1α and H-ferritin were shown to act on similar target populations of early BFU-E, CFU-GEMM, and CFU-GM. MIP-1β did not block the suppressive activity of H-ferritin. Also, hemin and an inactive recombinant human H-ferritin mutein counteracted the suppressive effects of the wildtype H-ferritin molecule, but did not block the suppressive effects of MIP-1α. These results show that MIP-1β's ability to block the action of MIP-1α is specific. In addition, the results suggest that MIP-1α and MIP-β can, through rapid action, modulate early myeloid progenitor cell proliferation.

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