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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1992-12-22
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pubmed:abstractText |
To determine the mechanism(s) by which interleukin-1 (IL-1) promotes granulopoiesis in vivo, we examined the effect of in vivo administration of IL-1 alpha on colony-stimulating factor (CSF) receptor expression on bone marrow cells (BMCs) and whether this directly correlated with progenitor cell responsiveness. Administration of IL-1 alpha to mice induced the upregulation of both granulocyte-macrophage-CSF (GM-CSF) and IL-3 receptors, which reached a maximum 24 hours after IL-1 alpha injection on unfractionated BMCs. This upregulation was more pronounced on the progenitor-enriched cell population (lineage-negative [Lin(-)]). The enhanced GM-CSF and IL-3 receptor expression directly correlated with enhanced IL-3- or GM-CSF-induced growth of colony-forming unit-culture (CFU-c) or CFU-mixture (CFU-Mix; colonies containing macrophages, granulocytes, and erythroid cells). In addition, the absolute number of high proliferative potential-colony-forming cells (HPP-CFC) was increased fivefold. In contrast, granulocyte-CSF (G-CSF)-specific binding on unfractionated BMCs was rapidly (4 hours) reduced after IL-1 alpha administration and returned to control levels by 24 hours. This reduction correlated with IL-1 alpha-induced margination of mature granulocytes (RBC-8C5hi cells), which express high levels of G-CSF receptors. IL-1 alpha treatment did not affect G-CSF receptor expression on Lin- cells. Pretreatment of mice with anti-type I IL-1 receptor antibody blocked the IL-1 alpha-induced upregulation of GM-CSF and IL-3 receptor expression on BMCs. Taken together, as one possible mechanism, IL-1 alpha in vivo may stimulate the expression of functional GM-CSF and IL-3 receptors on BMCs indirectly, and, in concert with the induction of circulating CSF levels, may account for the ability of IL-1 alpha to stimulate hematopoiesis in vivo.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-3
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
80
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2486-94
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1384785-Animals,
pubmed-meshheading:1384785-Bone Marrow,
pubmed-meshheading:1384785-Bone Marrow Cells,
pubmed-meshheading:1384785-Cell Division,
pubmed-meshheading:1384785-Erythroid Precursor Cells,
pubmed-meshheading:1384785-Female,
pubmed-meshheading:1384785-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:1384785-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:1384785-Granulocytes,
pubmed-meshheading:1384785-Hematopoiesis,
pubmed-meshheading:1384785-Hematopoietic Stem Cells,
pubmed-meshheading:1384785-Interleukin-1,
pubmed-meshheading:1384785-Interleukin-3,
pubmed-meshheading:1384785-Kinetics,
pubmed-meshheading:1384785-Macrophages,
pubmed-meshheading:1384785-Mice,
pubmed-meshheading:1384785-Mice, Inbred C57BL,
pubmed-meshheading:1384785-Receptors, Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:1384785-Receptors, Interleukin-3,
pubmed-meshheading:1384785-Up-Regulation
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pubmed:year |
1992
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pubmed:articleTitle |
In vivo effect of interleukin-1 alpha on hematopoiesis: role of colony-stimulating factor receptor modulation.
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pubmed:affiliation |
Biological Response Modifiers, Program Resources, Inc/DynCorp, Inc, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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