Granulocyte-macrophage colony formation in vitro using human non-phagocytic bone marrow cells

1988 ◽  
Vol 188 (6) ◽  
pp. 405-409 ◽  
Author(s):  
N. Ohhara ◽  
S. Okamura ◽  
S. Hayashi ◽  
T. Otsuka ◽  
Y. Niho
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Macrophage Colony ◽  
Marrow Cells

scholarly journals Inhibition of human macrophage colony formation by interleukin 4.

1989 ◽  
Vol 170 (2) ◽  
pp. 577-582 ◽  
Author(s):  
J H Jansen ◽  
G J Wientjens ◽  
W E Fibbe ◽  
R Willemze ◽  
H C Kluin-Nelemans
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Direct Action ◽  
Colony Growth ◽  
Interleukin 4 ◽  
Human Macrophage ◽  
Macrophage Colony ◽  
Marrow Cells

We investigated the effects of human rIL-4 on in vitro hematopoiesis. A profound inhibition of macrophage colony formation by IL-4 was observed, whereas colony growth of other lineages was not affected. Inhibition of macrophage colony growth was not restricted to GM-CSF-induced colony growth but was also present in cultures stimulated with M-CSF. This inhibition was not only observed in cultures of light density bone marrow cells, but also in cultures of monocyte- and T lymphocyte-depleted bone marrow cells. Since a similar inhibition was observed in cultures of CD34+HLA-DR+-enriched bone marrow cells, a direct action of IL-4 on monocyte-committed progenitor cells is suggested.

scholarly journals Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro

Blood ◽  
1990 ◽  
Vol 76 (10) ◽  
pp. 1997-2004 ◽  
Author(s):  
A Srivastava ◽  
E Bruno ◽  
R Briddell ◽  
R Cooper ◽  
C Srivastava ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Replication ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Parvovirus B19 ◽  
Northern Analysis ◽  
Viral Dna ◽  
Viral Dna Replication ◽  
Marrow Cells

Abstract Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue- tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.

scholarly journals Effect of cimetidine on granulocyte-macrophage colony formation by normal and chronic renal failure bone marrow cells

1984 ◽  
Vol 26 (5) ◽  
pp. 741-743
Author(s):  
Taly Weinstein ◽  
Pnina Fishman ◽  
Baruch Klein ◽  
Joseph Levi ◽  
Meir Djaldetti
Keyword(s):  
Bone Marrow ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Macrophage Colony ◽  
Marrow Cells

scholarly journals Acquired amegakaryocytic thrombocytopenic purpura: a syndrome of diverse etiologies

Blood ◽  
1982 ◽  
Vol 60 (5) ◽  
pp. 1173-1178 ◽  
Author(s):  
R Hoffman ◽  
E Bruno ◽  
J Elwell ◽  
E Mazur ◽  
AM Gewirtz ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Additional Patient ◽  
Platelet Glycoprotein ◽  
Intrinsic Defect ◽  
Thrombocytopenic Purpura ◽  
Marrow Cells

Abstract The possible pathogenetic mechanisms responsible for the production of acquired amegakaryocytic thrombocytopenic purpura (AATP) were investigated in a group of patients with this disorder. Absence of megakaryocytes and small platelet glycoprotein-bearing mononuclear cells, as determined by immunochemical staining of patient marrows with an antisera to platelet glycoproteins, suggested that the defect in AATP occurs in an early progenitor cell of the megakaryocytic lineage. Using an in vitro clonal assay system for negakaryocytic progenitor cells or megakaryocyte colony-forming units (CFU-M), the proliferative capacity of AATP marrow cells was then assessed. Bone marrow cells from three of four patients formed virtually no megakaryocyte colonies, suggesting that in these individuals the AATP was due to an intrinsic defect in the CFU-M. Bone marrow cells from an additional patient, however, formed 12% of the normal numbers of colonies, providing evidence for at least partial integrity of the CFU-M compartment in this patient. Serum specimens from all six patients were screened for their capacity to alter in vitro megakaryocyte colony formation. Five of six sera enhanced colony formation in a stepwise fashion, demonstrating appropriately elevated levels of megakaryocyte colony- stimulating activity. The serum of the patient with partial integrity of the CFU-M compartment, however, stimulated colony formation only at low concentrations. At higher concentrations, this patient's serum actually inhibited the number of colonies cloned, suggesting the presence of a humoral inhibitor to CFU-M. Serum samples from all patients were further screened for such humoral inhibitors of megakaryocyte colony formation using a cytotoxicity assay. The patient whose serum was inhibitory to CFU-M at high concentrations was indeed found to have a complement-dependent serum IgG inhibitor that was cytotoxic to allogeneic and autologous marrow CFU-M but did not alter erythroid colony formation. These-studies suggest that AATP can be due to at least two mechanisms: either an intrinsic effect at the level of the CFU-M or a circulating cytotoxic autoantibody directed against the CFU-M.

scholarly journals Macrophage colony formation supported by purified CSF-1 and/or interleukin 3 in serum-free culture: evidence for hierarchical difference in macrophage colony-forming cells

Blood ◽  
1986 ◽  
Vol 67 (4) ◽  
pp. 859-864 ◽  
Author(s):  
K Koike ◽  
ER Stanley ◽  
JN Ihle ◽  
M Ogawa
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Culture System ◽  
Bone Marrow Cells ◽  
Serum Free ◽  
Interleukin 3 ◽  
Two Factors ◽  
Macrophage Colony ◽  
Cells Cultured ◽  
Marrow Cells

Abstract Using a serum-free culture system, we examined murine macrophage colony formation from bone marrow cells cultured in the presence of purified CSF-1, interleukin 3 (IL 3) or a combination of the two factors. CSF-1 supported macrophage and neutrophil-macrophage colony formation, whereas IL-3 supported the formation of various types of single lineage and multilineage colonies. CSF-1 supported more macrophage colonies from bone marrow cells of normal mice than IL 3, whereas in cultures of bone marrow cells of 5-fluorouracil-treated mice, IL 3 supported more macrophage colonies. A combination of CSF-1 and IL 3 resulted in granulocyte-macrophage (GM) colony formation that was equal to or greater than the sum of GM colony formation supported by the factors individually. The combination of CSF-1 and IL 3 resulted in significant increases in the size of both macrophage and neutrophil-macrophage colonies. Similar increases in colony size were observed when CSF-1 was added to cultures five days after incubation of marrow cells with IL 3. These data support the concept that some of the macrophage colony- forming cells that respond to IL 3 are more primitive than those that are sensitive to CSF-1.

scholarly journals Fundamental Studies on Granulocyte-Macrophage Colony Formation by Mouse Bone Marrow Cells

1986 ◽  
Vol 8 (2) ◽  
pp. 193-199
Author(s):  
Yuji YAMAGUCHl ◽  
Masahiro MISAGO ◽  
Makoto KIKUCHI ◽  
Shyozo CHIBA
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Macrophage Colony ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells
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