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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunopathogenesis of experimental allergic encephalomyelitis (EAE) is reviewed with special focus on the role of central nervous system fibrin deposition in the inflammatory cascade characterizing this autoimmune disease. Among rats sensitized to whole spinal cord or myelin basic protein of either guinea pig or bovine origin, there is a striking degree of concordance of perivascular fibrin deposits and occurrence of clinical paralytic signs. Neither paralytic signs nor fibrin deposition are temporally related to development of perivascular cellular infiltrates. Rats sensitized to neuroantigen and treated with ancrod, a polypeptide derived from the venom of Agkistrodon rhodostoma, develop profound hypofibrinogenemia, have a marked inhibition of fibrin deposition, and often exhibit no paralytic signs whatsoever. In contrast, cellular infiltrates are not demonstrably influenced by ancrod treatment. Activation of the clotting cascade at loci of developing immune injury of nervous tissue appears to result from and lead to increasing neurovascular permeability and accumulation of edema fluid. Distention of the extracellular space in central and peripheral nervous system tissues by edema fluid appears to be directly responsible for clinical abnormalities characterizing EAE in rats. Cellular infiltrates, on the other hand, appear to be an independent immune response to neuroantigenic sensitization.
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PMID:Experimental allergic encephalomyelitis: role of fibrin deposition in immunopathogenesis of inflammation in rats. 6 95

We have previously shown that astrocytes produce and secrete plasminogen activator (PA) and that this function is responsive to various modulating agents. When astrocyte conditioned medium (CM) is subjected to SDS-PAGE and PA activity localized by fibrin-agar gel overlay, the activity in the CM is found to comigrate with control t-PA. On affinity chromatography CM PA specifically binds to t-PA antibody. The latter also inhibits fibrinolytic activity of CM PA. When incubated with a fibrin clot, CM PA activity can be shown to bind to fibrin. These observations help identify the enzyme in astrocyte CM as t-PA. A possible role of astrocyte PA in myelin injury could provide an explanation for the previously observed correlation between fibrin deposition and demyelination as well as inhibition of demyelination by ancrod and heparin in experimental allergic encephalomyelitis.
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PMID:Characterization of astrocyte plasminogen activator. 311 79