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  • Electronic Resource  (2)
  • CSF  (1)
  • Cytofluorometry  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Comparative analysis of the influences of IL-1, IL-3 and GM-CSF on the commitment of granulocyte-macrophage progenitors in vitro (1991)
    Springer
    Annals of hematology 63 (1991), S. 242-248 
    Details
    ISSN: 1432-0584
    Keywords: Hematopoiesis ; GM-CSF ; IL-3 ; IL-1 ; Precursor cells ; Cytofluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our experiments were directed towards the detection of the influence of interleukin-1 (IL-1); interleukin-3 (IL-3), and granulocyte-macrophage colonystimulating factor (GM-CSF) on the generation of granulocyte-macrophage progenitor cells. We also set out to examine whether this process is connected with changes within the early precursor cell compartment. Bone marrow suspension cultures (12 days) supplemented with these cytokines were tested for the presence of GM colony-forming cells (GM-CFC) in a colony-forming unit assay. The percentage of CD 34+ and HLA-DR+ as well as the number of blasts and promyelocytes were estimated cytofluorometrically and morphologically. The proliferative effect of GM-CSF was associated with a net increase of GM-CFC and HLA-DR+ myeloid cells and a decrease in the percentage of CD 34+ early precursor cells. IL-3 acted similarly and also caused an absolute decrease of CD 34+ cells in the cultures. IL-1 did not stimulate the generation of blasts or GM-CFC but elevated the number of CD 34− as well as HLA-DR-expressing cells in the cultures. These results imply that GM-CSF supported the maintenance of hematopoiesis in vitro. The transition from early precursor cells to committed myeloid progenitor cells (GM-CFC) and more mature precursor cells (G-CFC, M-CFC) may be supported by GM-CSF without affecting the self-renewing capacity of CD 34+ early precursors. In contrast, the blast-generating and proliferation-inducing action of IL-3 is associated with a drop in the total number of CD 34+ stem cells. An efficient renewal of this population obviously depends on the presence of IL-1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01698372
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation of oxidative metabolism of granulocytes by recombinant granulocyte-macrophage-colony-stimulating-factor and a conditioned medium of a urinary bladder carcinoma cell line (1987)
    Springer
    Annals of hematology 54 (1987), S. 307-312 
    Details
    ISSN: 1432-0584
    Keywords: Granulocytes ; CSF ; Oxidative metabolism ; Bladder carcinoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neutrophils (PMN) are the major host defence cells protecting the body against invasion by microorganisms. Products of oxidative metabolism mediate PMN microbicidal and tumoricidal activity, but the mechanisms by which these pathways become activated are not well understood. The colony stimulating factors (CSF) are known to stimulate proliferation and differentiation of committed bone marrow stem cells. These regulators may probably play an important role in non specific resistance to infections. We studied the oxidative metabolism of neutrophils after stimulation with recombinant GM-CSF (r.GM-CSF) and the concentrated conditioned medium of the UBC-5637 cell line (UBC-CM) showing CSF activity. It could be demonstrated that the r.GM-CSF, as well as the UBC-CM, induce an activation of the neutrophil respiratory burst without any cofactors such as f-MLP, PMA, or zymosan. In addition, we observed an increase of the response to those stimulants in the presence of either r.GM-CSF or UBC-CM. These effects were not endotoxin-induced, since stimulation persisted after addition of Polymyxin B, which is known to inhibit the action of endotoxins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00320879
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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