Source:http://linkedlifedata.com/resource/pubmed/id/10226735
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1999-7-27
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pubmed:abstractText |
The CXC chemokine interleukin-8 induces rapid mobilization of hematopoietic progenitor cells in mice and monkeys. Antibodies against the beta 2-integrin leukocyte function-associated antigen-1 completely blocked interleukin-8-induced mobilization. This was not due to a direct effect on the hematopoietic progenitor cells, as leukocyte function-associated antigen-1 was found not to be expressed on hematopoietic progenitor cells. Additional experiments showed that interleukin-8 induces the rapid release of the metalloproteinase gelatinase B, concurrent with the mobilization of hematopoietic progenitor cells. Mobilization could be completely prevented by anti-gelatinase B antibodies. Because neutrophils express leukocyte function-associated antigen-1 and high affinity interleukin-8 receptors, and release gelatinase B upon stimulation with interleukin-8, we hypothesized that neutrophils are key mediators in interleukin-8-induced stem cell mobilization. Further studies showed that mobilization by interleukin-8 was completely absent in mice rendered neutropenic with anti-granulocytic antibodies. Taken together, these data are consistent with an essential role for neutrophils in interleukin-8-induced stem cell mobilization.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1065-6251
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
152-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
1999
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pubmed:articleTitle |
Mechanisms underlying hematopoietic stem cell mobilization induced by the CXC chemokine interleukin-8.
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pubmed:affiliation |
Department of Hematology, Leiden University Medical Center, The Netherlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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