Retroviruses induce granulocyte–macrophage colony stimulating activity in fibroblasts

Nature ◽  
1982 ◽  
Vol 299 (5884) ◽  
pp. 638-640 ◽  
Author(s):  
Mark J. Koury ◽  
Ian B. Pragnell
Keyword(s):  
Colony Stimulating Activity ◽  
Macrophage Colony

Murine osteoblastlike cells and the osteogenic cell MC3T3-E1 release a macrophage colony-stimulating activity in culture

1987 ◽  
Vol 41 (3) ◽  
pp. 151-156 ◽  
Author(s):  
P. R. Elford ◽  
R. Felix ◽  
M. Cecchini ◽  
U. Trechsel ◽  
H. Fleisch
Keyword(s):  
Osteogenic Cell ◽  
Colony Stimulating Activity ◽  
Macrophage Colony

In vitro production of granulocyte–macrophage colony-stimulating activity by murine bone marrow and spleen following vinblastine administrationIN VIVO

1987 ◽  
Vol 5 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Douglas E. Williams ◽  
David S. Chervinsky ◽  
Frank R. Orsini ◽  
Cameron K. Tebbi ◽  
John E. Fitzpatrick
Keyword(s):  
Bone Marrow ◽  
In Vitro Production ◽  
Murine Bone Marrow ◽  
Colony Stimulating Activity ◽  
Macrophage Colony ◽  
Vitro Production

scholarly journals Human macrophage colony-stimulating factor induces macrophage colonies after L-phenylalanine methylester treatment of human marrow

Blood ◽  
1990 ◽  
Vol 76 (9) ◽  
pp. 1783-1787 ◽  
Author(s):  
CS Rosenfeld ◽  
C Evans ◽  
RK Shadduck
Keyword(s):  
Bone Marrow ◽  
Conditioned Media ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Human Macrophage ◽  
Colony Stimulating Factor ◽  
Colony Stimulating Activity ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Macrophage-colony stimulating factor (M-CSF) has well-known effects on murine bone marrow, but its colony stimulating activity for human bone marrow is controversial. After treatment of human bone marrow with L- phenylalanine methylester (PME), macrophage-colonies (CFU-M) were induced by M-CSF in a dose-dependent fashion. The optimal concentration of recombinant human-macrophage colony stimulating factor (rhM-CSF) was 1,000 U/mL. Purified human urine M-CSF had colony stimulating activity similar to rhM-CSF. Further studies were performed to determine the factors responsible for the enhanced CFU-M formation from PME treated marrow. Compared with nylon wool and carbonyl iron monocyte depletion methods, PME eliminated significantly more monocytes and myeloid cells. This observation suggested that these cells may release hematopoietic inhibitory factors for CFU-M. Low concentrations (1%) but not normal (10%) concentrations of blood monocytes were inhibitory (mean inhibition, 48%) to CFU-M. High concentrations of monocytes (50%) augmented CFU-M colonies. HL-60 conditioned media was used to simulate secretory products of early myeloid cells. HL-60 conditioned media (1%) inhibited CFU-M formation but not granulocyte macrophage or granulocyte colonies. We conclude that M-CSF has colony stimulating activity for human marrow that can be recognized after removal of inhibitory cells by PME treatment.

scholarly journals Contrasting patterns of DNA strand breakage and ADP-ribosylation- dependent DNA ligation during granulocyte and monocyte differentiation

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1114-1119 ◽  
Author(s):  
Z Khan ◽  
GE Francis
Keyword(s):  
Structural Changes ◽  
Dna Supercoiling ◽  
Monocytic Differentiation ◽  
Dna Breaks ◽  
Strand Breaks ◽  
Colony Stimulating Activity ◽  
Strand Breakage ◽  
Macrophage Colony ◽  
Dna Strand ◽  
Dna Strand Breakage

Previous studies have shown that structural changes in DNA, including the ligation of pre-existing DNA breaks and the opening and closure of new breaks, occur shortly after exposure of granulomonocytic precursors (CFU-GM) to granulocyte-macrophage colony stimulating activity (GM- CSA). Monocytic differentiation of CFU-GM is selectively inhibited by compounds known to inhibit the nuclear enzyme ADP-ribosyl transferase (ADPRT). Since this enzyme, which transfers ADP-ribose units to chromatin proteins, is known to activate DNA ligase, we attempted to determine whether ligation of one or both types of DNA break is required for monocytic differentiation. Breaks in DNA were examined using the nucleoid sedimentation technique in which DNA breaks cause loss of DNA supercoiling in nucleoids and concomitant changes in their sedimentation through neutral sucrose gradients. We here report that two distinct patterns of DNA strand breakage and ligation are associated with differentiation to the granulocyte and monocyte lineages. Monocytic inducers (phorbolester and vitamin D3) predominantly produce closure of pre-existing strand breaks, whereas granulocytic inducers (granulocyte colony stimulating activity, G-CSA; retinoic acid) cause opening and closure of new breaks. Only ligation of the pre-existing breaks is highly sensitive to inhibition by 3- methoxybenzamide (a potent ADPRT inhibitor), and only monocytic differentiation is impaired by addition of this compound. These findings suggest that DNA structural changes may be directly involved in granulocyte-macrophage switching.

scholarly journals Granulocyte macrophage colony-stimulating activity production by cultured human thymic nonlymphoid cells is regulated by endogenous interleukin-1

Blood ◽  
1988 ◽  
Vol 72 (4) ◽  
pp. 1230-1236
Author(s):  
D Ridgway ◽  
MS Borzy ◽  
GC Bagby
Keyword(s):  
Mononuclear Cells ◽  
Marrow Cell ◽  
Interleukin 1 ◽  
Colony Growth ◽  
Gm Csf ◽  
Colony Stimulating Activity ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Cell Conditioned Medium

Supernatants of cultured human thymic nonlymphoid cells were assayed for granulopoietic factors using cultures of low density bone marrow mononuclear cells (LD-BMMC). Thymic nonlymphoid cell-conditioned medium (TNLC-CM) supported vigorous myeloid colony growth of LD-BMMC, and of LD-BMMC depleted of T lymphocytes and/or monocytes. Colony stimulating activity (CSA) in TNLC-CM was abrogated by a highly specific neutralizing antiserum against recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF). TNLC-CM also enhanced colony growth in LD-BMMC stimulated by colony stimulating activity from a giant cell tumor culture (GCT). The enhancing activity of TNLC-CM, unlike its CSA activity, required the presence of adherent cells in the marrow cell culture. The addition of anti-interleukin-1 (anti-IL-1) antibody to TNLC-CM inhibited the GCT-enhancing activity, but not the CSA. When the anti-IL-1 immunoglobulin was added directly to cultures of thymic nonlymphoid cells, GM-CSF production was completely inhibited, and the GCT enhancing activity was neutralized. We conclude that an intercellular regulatory network exists in cultured thymic explants in which GM-CSF expression is induced by IL-1. In this system, the granulopoietic effect of IL-1 derives not from a direct effect on myeloid progenitors, but from its ability to recruit CSA production by other cells.

scholarly journals Human macrophage colony-stimulating factor induces macrophage colonies after L-phenylalanine methylester treatment of human marrow

Blood ◽  
1990 ◽  
Vol 76 (9) ◽  
pp. 1783-1787
Author(s):  
CS Rosenfeld ◽  
C Evans ◽  
RK Shadduck
Keyword(s):  
Bone Marrow ◽  
Conditioned Media ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Human Macrophage ◽  
Colony Stimulating Factor ◽  
Colony Stimulating Activity ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Macrophage-colony stimulating factor (M-CSF) has well-known effects on murine bone marrow, but its colony stimulating activity for human bone marrow is controversial. After treatment of human bone marrow with L- phenylalanine methylester (PME), macrophage-colonies (CFU-M) were induced by M-CSF in a dose-dependent fashion. The optimal concentration of recombinant human-macrophage colony stimulating factor (rhM-CSF) was 1,000 U/mL. Purified human urine M-CSF had colony stimulating activity similar to rhM-CSF. Further studies were performed to determine the factors responsible for the enhanced CFU-M formation from PME treated marrow. Compared with nylon wool and carbonyl iron monocyte depletion methods, PME eliminated significantly more monocytes and myeloid cells. This observation suggested that these cells may release hematopoietic inhibitory factors for CFU-M. Low concentrations (1%) but not normal (10%) concentrations of blood monocytes were inhibitory (mean inhibition, 48%) to CFU-M. High concentrations of monocytes (50%) augmented CFU-M colonies. HL-60 conditioned media was used to simulate secretory products of early myeloid cells. HL-60 conditioned media (1%) inhibited CFU-M formation but not granulocyte macrophage or granulocyte colonies. We conclude that M-CSF has colony stimulating activity for human marrow that can be recognized after removal of inhibitory cells by PME treatment.

scholarly journals Human serum megakaryocyte colony-stimulating activity appears to be distinct from interleukin-3, granulocyte-macrophage colony-stimulating factor, and lymphocyte-conditioned medium

Blood ◽  
1990 ◽  
Vol 76 (2) ◽  
pp. 290-297 ◽  
Author(s):  
EM Mazur ◽  
JL Cohen ◽  
J Newton ◽  
P Sohl ◽  
A Narendran ◽  
...  
Keyword(s):  
Human Serum ◽  
Conditioned Medium ◽  
Colony Growth ◽  
Colony Stimulating Factor ◽  
Interleukin 3 ◽  
Gm Csf ◽  
Colony Stimulating Activity ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Sera from patients with bone marrow megakaryocyte aplasia are a rich source of megakaryocyte colony-stimulating activity (Meg-CSA). Other biologic materials exhibiting Meg-CSA include phytohemagglutinin- stimulated human lymphocyte-conditioned medium (PHA-LCM), recombinant interleukin-3 (IL-3), and recombinant granulocyte macrophage colony- stimulating factor (GM-CSF). Neutralizing antisera to both recombinant IL-3 and GM-CSF were used to evaluate the relationship among these sources of Meg-CSA. Varying dilutions of IL-3 and GM-CSF antisera were tested in plasma clot cultures of normal human peripheral blood megakaryocyte progenitors optimally stimulated by either IL-3 (1 U/mL), GM-CSF (1 U/mL), PHA-LCM (2.5% to 5% vol/vol), or aplastic human serum (10% vol/vol). IL-3 antiserum at dilutions up to 1/2,000 totally abrogated megakaryocyte colony growth stimulated by IL-3. A 1/500 dilution of GM-CSF antiserum completely eliminated GM-CSF-induced megakaryocyte colony development. A combination of anti-IL-3 and anti- GM-CSF, each at a 1/500 dilution, inhibited all megakaryocyte colony growth stimulated by optimal concentrations of IL-3 and GM-CSF together. There was no neutralizing crossreactivity between the IL-3 and GM-CSF antisera. At maximally neutralizing concentrations, IL-3 antiserum inhibited 66% of the megakaryocyte colony growth stimulated by PHA-LCM. Residual megakaryocyte colony growth was eliminated by the addition of a 1/500 dilution of anti-GM-CSF.

scholarly journals Specificity of lactoferrin as an inhibitor of granulocyte-macrophage colony-stimulating activity production from fetal mouse liver cells

Blood ◽  
1979 ◽  
Vol 54 (4) ◽  
pp. 951-954 ◽  
Author(s):  
JR Zucali ◽  
HE Broxmeyer ◽  
JA Ulatowski
Keyword(s):  
Mouse Liver ◽  
Liver Cells ◽  
Inhibiting Activity ◽  
Fetal Mouse ◽  
Colony Stimulating Activity ◽  
Fetal Mouse Liver ◽  
Macrophage Colony

Abstract Fetal mouse liver cultures capable of producing both erythropoietin (Ep) and granulocyte-macrophage colony stimulating activity (GM-CSA) were used to study the specificity of lactoferrin as an inhibitor of the production of GM-CSA. Both a granulocyte-derived colony-inhibiting activity (CIA) and lactoferrin inhibited GM-CSA production while having no effect on Ep production. These results demonstrate the specificity of lactoferrin for GM-CSA production.

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