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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2001-6-11
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pubmed:abstractText |
The role of selectins in neutrophil emigration in response to the CXC chemokines KC and MIP-2 was investigated in wild type and P-selectin deficient mice. Intrapleural injection of KC or MIP-2 induced a rapid and specific neutrophil accumulation. Emigration 2 h after KC or MIP-2 was reduced 83 - 88% by anti-L-selectin mAb and 53 - 63% by anti-P-selectin mAb. Co-administration of anti-L- and P-selectin mAbs abolished neutrophil migration induced by either chemokine. An anti-E-selectin mAb tested alone did not affect KC-induced neutrophil migration after 2 or 4 h. Moreover, anti-E-selectin did not have an additive inhibitory effect on KC-induced neutrophil migration compared with P-selectin blockade alone. This was found when neutrophil migration was measured at 2 and 4 h after KC. Despite a blood neutrophilia, neutrophil migration at 2 and 4 h after KC was markedly smaller (by approximately 90%) in P-selectin deficient mice compared with wild type animals. Responses at both time points were not decreased further in animals given E-selectin mAb but were reduced to the PBS control level in the presence of anti-L-selectin. In vitro study of cultured murine endothelial cells demonstrated that KC can directly increase cell surface P-selectin expression. These data suggest that CXC chemokine-induced neutrophil accumulation is dependent on both neutrophil L-selectin and a rapid upregulation of endothelial P-selectin but there is no evidence for E-selectin induction.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-1379089,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-1379593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-1713222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-1840701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-1986307,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-2194589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-2551036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-6866086,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7508943,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7520302,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7521884,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7522403,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7636213,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7636264,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7689836,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7751647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7883948,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-7961909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-8288247,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-9317159,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11399672-9692902
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL1,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/Chemotactic Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/L-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/P-Selectin
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0007-1188
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
133
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
550-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11399672-Animals,
pubmed-meshheading:11399672-Cell Movement,
pubmed-meshheading:11399672-Chemokine CXCL1,
pubmed-meshheading:11399672-Chemokine CXCL2,
pubmed-meshheading:11399672-Chemokines,
pubmed-meshheading:11399672-Chemokines, CXC,
pubmed-meshheading:11399672-Chemotactic Factors,
pubmed-meshheading:11399672-Dose-Response Relationship, Drug,
pubmed-meshheading:11399672-E-Selectin,
pubmed-meshheading:11399672-Endothelium, Vascular,
pubmed-meshheading:11399672-Growth Substances,
pubmed-meshheading:11399672-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:11399672-L-Selectin,
pubmed-meshheading:11399672-Mice,
pubmed-meshheading:11399672-Mice, Inbred BALB C,
pubmed-meshheading:11399672-Mice, Inbred C57BL,
pubmed-meshheading:11399672-Neutrophils,
pubmed-meshheading:11399672-P-Selectin,
pubmed-meshheading:11399672-Pleura,
pubmed-meshheading:11399672-Time Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Dominant role of L- and P-selectin in mediating CXC chemokine-induced neutrophil migration in vivo.
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pubmed:affiliation |
Endothelial Cell Biology Laboratory, Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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