Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-11-22
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
587-96
pubmed:dateRevised
2006-11-15
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
pubmed:year
1996
pubmed:articleTitle
Complement activation in the central nervous system following blood-brain barrier damage in man.
pubmed:affiliation
Department of Neurology, University of Helsinki, Finland.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't