Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1992-12-22
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2486-94
pubmed:dateRevised
2008-11-21
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
pubmed:year
1992
pubmed:articleTitle
In vivo effect of interleukin-1 alpha on hematopoiesis: role of colony-stimulating factor receptor modulation.
pubmed:affiliation
Biological Response Modifiers, Program Resources, Inc/DynCorp, Inc, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.