Source:http://linkedlifedata.com/resource/pubmed/id/11031083
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-11-17
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pubmed:abstractText |
The inflammatory response that ensues during the initial 48 to 72 h after spinal cord injury causes considerable secondary damage to neurons and glia. Infiltration of proinflammatory-activated neutrophils and monocytes/macrophages into the cord contributes to spinal cord injury-associated secondary damage. beta2 integrins play an essential role in leukocyte trafficking and activation and arbitrate cell-cell interactions during inflammation. The beta2 integrin, alphaDbeta2, is expressed on monocytes/macrophages and neutrophils and binds to vascular adhesion molecule-1 (VCAM-1). The increased expression of VCAM-1 during central nervous system (CNS) inflammation likely contributes to leukocyte extravasation into the CNS. Accordingly, blocking the interaction between alphaDbeta2 and VCAM-1 may attenuate the inflammatory response at the SCI site. We investigated whether the administration of monoclonal antibodies (mAbs) specific for the rat alphaD subunit would reduce the inflammatory response after a spinal cord transection injury in rats. At a 1 mg/kg dose two of three anti-alphaD mAbs caused a significant ( approximately 65%) reduction in the number of macrophages at the injury site and one anti-alphaD mAb led to a approximately 43% reduction in the number of neutrophils at the SCI site. Thus, our results support the concept that the alphaDbeta2 integrins play an important role in the trafficking of leukocytes to a site of central nervous system inflammation. This study also offers preliminary evidence that anti-alphaD mAbs can reduce the extravasation of macrophages and, to a lesser extent, neutrophils, to the SCI site.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11,
http://linkedlifedata.com/resource/pubmed/chemical/ITGAD protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Integrin alpha Chains,
http://linkedlifedata.com/resource/pubmed/chemical/Integrins,
http://linkedlifedata.com/resource/pubmed/chemical/Methylprednisolone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoadhesin,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0014-4886
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 Academic Press.
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pubmed:issnType |
Print
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pubmed:volume |
166
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
52-64
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11031083-Animals,
pubmed-meshheading:11031083-Antigens, CD11,
pubmed-meshheading:11031083-Cell Movement,
pubmed-meshheading:11031083-Disease Models, Animal,
pubmed-meshheading:11031083-Integrin alpha Chains,
pubmed-meshheading:11031083-Integrins,
pubmed-meshheading:11031083-Macrophages,
pubmed-meshheading:11031083-Male,
pubmed-meshheading:11031083-Methylprednisolone,
pubmed-meshheading:11031083-Monocytes,
pubmed-meshheading:11031083-Myelitis,
pubmed-meshheading:11031083-Neutrophils,
pubmed-meshheading:11031083-Rats,
pubmed-meshheading:11031083-Rats, Wistar,
pubmed-meshheading:11031083-Receptors, Cytoadhesin,
pubmed-meshheading:11031083-Spinal Cord Injuries,
pubmed-meshheading:11031083-Vascular Cell Adhesion Molecule-1
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pubmed:year |
2000
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pubmed:articleTitle |
Inhibition of monocyte/macrophage migration to a spinal cord injury site by an antibody to the integrin alphaD: a potential new anti-inflammatory treatment.
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pubmed:affiliation |
The Neurodegeneration Research Group, The John P. Robarts Research Institute, London, Ontario, N6A 5K8, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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