scholarly journals Evidence of the existence of a factor that induces Fc receptors on bone marrow cells

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 756-760 ◽  
Author(s):  
M Calcagno ◽  
JR Perez ◽  
MG Waldo ◽  
G Cabrera ◽  
B Weiss-Steider

Abstract The existence of a molecule responsible for the induction of Fc receptor (FcR) on bone marrow cells (FcR inducer, FcRI) is demonstrated in conditioned media from the macrophage-like cell line WR19M.1 activated by bacterial lipopolysaccharides. The molecular weight obtained from molecular sieving chromatography in gel and density gradient sedimentation is found to be 18,500 daltons and 16,000 daltons, respectively, with an isoelectric pH of 7.4. The factor is found to be thermolabile and trypsin sensitive. The macrophage and granulocyte inducer (MGI), also known as colony-stimulating factor (CSF) or colony-stimulating activity (CSA), is identified from the same source and found to have a molecular weight and an isoelectric pH different from FcRI. The fractions that contained the MGI did not induce FcR on bone marrow cells, while the fractions rich in FcRI did not induce colony formation.

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 756-760
Author(s):  
M Calcagno ◽  
JR Perez ◽  
MG Waldo ◽  
G Cabrera ◽  
B Weiss-Steider

The existence of a molecule responsible for the induction of Fc receptor (FcR) on bone marrow cells (FcR inducer, FcRI) is demonstrated in conditioned media from the macrophage-like cell line WR19M.1 activated by bacterial lipopolysaccharides. The molecular weight obtained from molecular sieving chromatography in gel and density gradient sedimentation is found to be 18,500 daltons and 16,000 daltons, respectively, with an isoelectric pH of 7.4. The factor is found to be thermolabile and trypsin sensitive. The macrophage and granulocyte inducer (MGI), also known as colony-stimulating factor (CSF) or colony-stimulating activity (CSA), is identified from the same source and found to have a molecular weight and an isoelectric pH different from FcRI. The fractions that contained the MGI did not induce FcR on bone marrow cells, while the fractions rich in FcRI did not induce colony formation.


Blood ◽  
1990 ◽  
Vol 75 (12) ◽  
pp. 2286-2291 ◽  
Author(s):  
K Koike ◽  
T Nakahata ◽  
T Kubo ◽  
T Kikuchi ◽  
M Takagi ◽  
...  

We investigated the effect of interleukin-6 (IL-6) on murine megakaryocytopoiesis in a serum-free culture system. The addition of IL- 6 to a culture containing interleukin-3 (IL-3) resulted in a significant increase in the number of megakaryocyte colonies by bone marrow cells of normal mice. The megakaryocytic progenitors that survive exposure to 5-fluorouracil (5-FU) exhibited a more significant response to IL-6 and IL-3. Polyclonal anti-IL-6 antibody neutralized the stimulatory effect of IL-6 on megakaryocyte colony growth supported by IL-3. Delayed addition experiments and replating experiments of blast cell colonies showed that megakaryocytic progenitors are supported by IL-3 in the early stage of the development but require IL- 6 for their subsequent proliferation and differentiation. In addition, IL-6 increased the size of megakaryocytes in granulocyte-macrophage- megakaryocyte colonies. The combination of granulocyte colony- stimulating factor or granulocyte-macrophage colony stimulating factor with IL-3 resulted in an increase in the granulocyte-macrophage colony growth of bone marrow cells of 5-FU-treated mice or normal mice, respectively, but had little effect on the enhancement of pure and mixed megakaryocyte colony growth. These results suggest that IL-6 plays an important role in murine megakaryocytopoiesis.


Blood ◽  
1997 ◽  
Vol 89 (4) ◽  
pp. 1165-1172 ◽  
Author(s):  
Russell S. Taichman ◽  
Marcelle J. Reilly ◽  
Rama S. Verma ◽  
Stephen G. Emerson

Abstract Based on anatomic and developmental findings characterizing hematopoietic cells in close approximation with endosteal cells, we have begun an analysis of osteoblast/hematopoietic cell interactions. We explore here the functional interdependence between these two cell types from the standpoint of de novo cytokine secretion. We determined that, over a 96-hour period, CD34+ bone marrow cells had no significant effect on osteoblast secretion of granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, or transforming growth factor-β1 , but in some experiments minor increases in leukemia inhibitory factor levels were observed. However, when CD34+ bone marrow cells were cocultured in direct contact with osteoblasts, a 222% ± 55% (range, 153% to 288%) augmentation in interleukin-6 (IL-6) synthesis was observed. The accumulation of IL-6 protein was most rapid during the initial 24-hour period, accounting for nearly 55% of the total IL-6 produced by osteoblasts in the absence of blood cells and 77% of the total in the presence of the CD34+ cells. Cell-to-cell contact does not appear to be required for this activity, as determined by coculturing the two cell types separated by porous micromembranes. The identity of the soluble activity produced by the CD34+ cells remains unknown, but is not likely due to IL-1β or tumor necrosis factor-α, as determined with neutralizing antibodies. To our knowledge, these data represent the first demonstration that early hematopoietic cells induce the production of molecules required for the function of normal bone marrow microenvironments, in this case through the induction of hematopoietic cytokine (IL-6) secretion by osteoblasts.


Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 408-420 ◽  
Author(s):  
G Pigoli ◽  
A Waheed ◽  
RK Shadduck

Abstract Radioiodinated L-cell-derived colony-stimulating factor (CSF) was used to characterize the binding reaction to murine bone marrow cells. The major increment in cell-associated radioactivity occurred over 24 hr incubation at 37 degrees C, but virtually no binding was observed at 4 degrees C. The reaction was saturable with approximately 1 ng/ml of purified CSF. Unlabeled CSF prevented the binding, whereas a number of other hormones and proteins did not compete for CSF uptake. Further specificity studies showed virtually no binding to human bone marrow, which is unresponsive to this form of murine CSF. Minimal CSF uptake was noted with murine peritoneal macrophages, but virtually no binding was detected with thymic, lymph node, liver, or kidney cells. The marrow cell interaction with tracer appeared to require a new protein synthesis, as the binding was prevented by cycloheximide or puromycin. Preincubation of marrow cells in medium devoid of CSF increased the degree of binding after 1 hr exposure to the tracer. This suggests that CSF binding sites may be occupied or perhaps decreased in response to ambient levels of CSF in vivo. Approximately 70% of the bound radioactivity was detected in the cytoplasm at 24 hr. This material was partially degraded as judged by a decrease in molecular weight from approximately 62,000 to 2 peaks of approximately 32,000 and approximately 49,000, but 72% of the binding activity was retained. After plateau binding was achieved, greater than 80% of the radioactivity released into the medium was degraded into biologically inactive peptides with molecular weights less than 10,000. These findings suggest that the interaction of CSF with marrow cells is characterized by binding with subsequent internalization and metabolic degradation into portions of the molecule that are devoid of biologic activity.


Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 597-601 ◽  
Author(s):  
Y Yamamoto-Yamaguchi ◽  
M Tomida ◽  
M Hozumi

Abstract The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony- stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.


Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 597-601 ◽  
Author(s):  
Y Yamamoto-Yamaguchi ◽  
M Tomida ◽  
M Hozumi

The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony- stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.


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