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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1996-11-22
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pubmed:abstractText |
The central nervous system (CNS) is virtually isolated from circulating immunological factors such as complement (C), an important mediator of humoral immunity and inflammation. In circulation, C is constantly inhibited to prevent attack on host cells. Since a host of diseases produce an abnormal blood-brain/cerebrospinal fluid (blood-brain/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hemorrhage (SAH) or brain infarction. After SAH (n = 15), the terminal complement complex (TCC) concentration on days 0 to 2 was higher in the CSF, 210 +/- 61 ng/ml, than in the plasma, 63 +/- 17 ng/ml, but null in the CSF of controls (n = 8) or patients with an ischemic stroke (n = 7). TCC was eliminated from the CSF after SAH (24 +/- 10 ng/ml on days 7 to 10). Incubation of normal human CSF with serum in vitro also activated the terminal C pathway. In 10 fatal ischemic brain infarctions, immunohistochemical techniques demonstrated neuronal fragment-associated deposition of C9 accompanied by neutrophil infiltration. We conclude that the C system becomes activated intrathecally in SAH and focally in the brain parenchyma in ischemic stroke. By promoting chemotaxis and vascular perturbation, C activation may instigate nonimmune inflammation and aggravate CNS damage in diseases associated with plasma extravasation.
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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/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Betamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Membrane Attack Complex,
http://linkedlifedata.com/resource/pubmed/chemical/Edetic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Nimodipine,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0364-5134
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
587-96
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8871578-Adult,
pubmed-meshheading:8871578-Aneurysm, Ruptured,
pubmed-meshheading:8871578-Anti-Inflammatory Agents,
pubmed-meshheading:8871578-Betamethasone,
pubmed-meshheading:8871578-Blood-Brain Barrier,
pubmed-meshheading:8871578-Brain,
pubmed-meshheading:8871578-Chemotaxis,
pubmed-meshheading:8871578-Complement Activation,
pubmed-meshheading:8871578-Complement Membrane Attack Complex,
pubmed-meshheading:8871578-Edetic Acid,
pubmed-meshheading:8871578-Extravasation of Diagnostic and Therapeutic Materials,
pubmed-meshheading:8871578-Female,
pubmed-meshheading:8871578-Humans,
pubmed-meshheading:8871578-Immunohistochemistry,
pubmed-meshheading:8871578-Male,
pubmed-meshheading:8871578-Middle Aged,
pubmed-meshheading:8871578-Neutrophils,
pubmed-meshheading:8871578-Nimodipine,
pubmed-meshheading:8871578-Subarachnoid Hemorrhage,
pubmed-meshheading:8871578-Tomography, X-Ray Computed,
pubmed-meshheading:8871578-Vasodilator Agents
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pubmed:year |
1996
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pubmed:articleTitle |
Complement activation in the central nervous system following blood-brain barrier damage in man.
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pubmed:affiliation |
Department of Neurology, University of Helsinki, Finland.
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pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro,
Research Support, Non-U.S. Gov't
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