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rdf:type |
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lifeskim:mentions |
umls-concept:C0006104,
umls-concept:C0009506,
umls-concept:C0015376,
umls-concept:C0027950,
umls-concept:C0032214,
umls-concept:C0035820,
umls-concept:C0056196,
umls-concept:C0231491,
umls-concept:C0332206,
umls-concept:C1280500,
umls-concept:C1511545
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pubmed:issue |
1-2
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pubmed:dateCreated |
2004-9-2
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pubmed:abstractText |
The role of complement components in traumatic brain injury is poorly understood. Here we show that secondary damage after acute cryoinjury is significantly reduced in C3-/- or C5-/- mice or in mice treated with C5a receptor antagonist peptides. Injury sizes and neutrophil extravasation were compared. While neutrophil density increased following traumatic brain injury in wild type (C57BL/6) mice, C3-deficient mice demonstrated lower neutrophil extravasation and injury sizes in the brain. RNase protection assay indicated that C3 contributes to the induction of brain inflammatory mediators, MIF, RANTES (CCL5) and MCP-1 (CCL2). Intracranial C3 injection induced neutrophil extravasation in injured brains of C3-/- mice suggesting locally produced C3 is important in brain inflammation. We show that neutrophil extravasation is significantly reduced in both C5-/- mice and C5a receptor antagonist treated cryoinjured mice suggesting that one of the possible mechanisms of C3 effect on neutrophil extravasation is mediated via downstream complement activation products such as C5a. Our data indicates that complement inhibitors may ameliorate traumatic brain injury.
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pubmed:grant |
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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 CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL5,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Intramolecular Oxidoreductases,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Migration-Inhibitory...,
http://linkedlifedata.com/resource/pubmed/chemical/Mif protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Anaphylatoxin C5a
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0165-5728
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2004 Elsevier B.V.
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pubmed:issnType |
Print
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pubmed:volume |
155
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
55-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15342196-Animals,
pubmed-meshheading:15342196-Brain Injuries,
pubmed-meshheading:15342196-Chemokine CCL2,
pubmed-meshheading:15342196-Chemokine CCL5,
pubmed-meshheading:15342196-Chemotaxis, Leukocyte,
pubmed-meshheading:15342196-Cold Temperature,
pubmed-meshheading:15342196-Complement C3,
pubmed-meshheading:15342196-Complement C5,
pubmed-meshheading:15342196-Disease Models, Animal,
pubmed-meshheading:15342196-Inflammation Mediators,
pubmed-meshheading:15342196-Intramolecular Oxidoreductases,
pubmed-meshheading:15342196-Macrophage Migration-Inhibitory Factors,
pubmed-meshheading:15342196-Mice,
pubmed-meshheading:15342196-Mice, Inbred C57BL,
pubmed-meshheading:15342196-Mice, Knockout,
pubmed-meshheading:15342196-Neutrophils,
pubmed-meshheading:15342196-Peptides,
pubmed-meshheading:15342196-RNA, Messenger,
pubmed-meshheading:15342196-Receptor, Anaphylatoxin C5a
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pubmed:year |
2004
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pubmed:articleTitle |
Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist.
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pubmed:affiliation |
Department of Pathology, University of Wisconsin-Madison, 1300 University Ave, Madison, WI 53706, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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