Source:http://linkedlifedata.com/resource/pubmed/id/11591793
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2001-10-9
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pubmed:abstractText |
Macrophage-inflammatory protein 2 (MIP-2) is a major CXC chemokine involved in the migration of polymorphonuclear neutrophils (PMNs) to sites of inflammation. Although cell culture experiments have identified different cell types that can produce MIP-2, the cellular sources in vivo are not clearly defined. By using immunohistochemical staining and analysis of chemokine mRNA expression, the present study aimed to localize cells producing MIP-2 in tissues of normal mice and mice challenged with Yersinia enterocolitica. The results showed a constitutive expression of MIP-2 mRNA in bone marrow (BM) of normal mice, but not in other organs such as spleen, lung, or liver. MIP-2 protein was found in all organs tested but it was exclusively associated with PMNs that stained positive with the cell surface marker Gr-1. Bacterial infection caused a 5-fold increase in the number of MIP-2-positive PMNs recruited to spleens concomitant with a strong increase of splenic MIP-2 mRNA. This correlated well with a 3-fold loss of MIP-2-producing cells in BM. Because MIP-2 mRNA expression in PMNs was increased after stimulation with TNF, the results indicate that newly recruited PMNs can supplement their MIP-2 content through TNF-stimulated transcription. Together, the data imply a constitutive production of MIP-2 by a subset of PMNs in BM and argue for the possibility of a rapid mobilization of MIP-2 through its storage in circulating PMNs.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4635-43
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11591793-Animals,
pubmed-meshheading:11591793-Bone Marrow Cells,
pubmed-meshheading:11591793-Chemokine CXCL2,
pubmed-meshheading:11591793-Chemokines,
pubmed-meshheading:11591793-Chemotaxis, Leukocyte,
pubmed-meshheading:11591793-Female,
pubmed-meshheading:11591793-Granulocytes,
pubmed-meshheading:11591793-Interleukin-1,
pubmed-meshheading:11591793-Leukopoiesis,
pubmed-meshheading:11591793-Mice,
pubmed-meshheading:11591793-Mice, Inbred BALB C,
pubmed-meshheading:11591793-Neutrophils,
pubmed-meshheading:11591793-RNA, Messenger,
pubmed-meshheading:11591793-Spleen,
pubmed-meshheading:11591793-Tissue Distribution,
pubmed-meshheading:11591793-Tumor Necrosis Factor-alpha,
pubmed-meshheading:11591793-Yersinia Infections,
pubmed-meshheading:11591793-Yersinia enterocolitica
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pubmed:year |
2001
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pubmed:articleTitle |
Constitutive expression of macrophage-inflammatory protein 2 (MIP-2) mRNA in bone marrow gives rise to peripheral neutrophils with preformed MIP-2 protein.
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pubmed:affiliation |
Institute for Clinical Microbiology, Immunology, and Hygiene, University of Erlangen, Erlangen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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