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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary segmental demyelination accompanied by mononuclear phagocytes was induced by injection of antiserum into rat peripheral nerve, and the morphologic sequence of events was studied. Antisera were obtained from rabbits with experimental allergic neuritis (EAN) produced by the inoculation of emulsified bovine peripheral nerves in complete Freund's adjuvant. Sera were injected directly into rat sciatic nerve to circumvent the blood-nerve barrier. Recipient rats developed sensorimotor paralysis on the side injected with experimental allergic neuritis sera. Intense focal demyelinative lesions resulted from injection of experimental allergic neuritis sera. Control sera obtained from rabbits inoculated with bovine serum albumin in complete Freund's adjuvant did not produce paralysis or demyelination. The earliest change was damage to Schwann cells, seen 20 minutes after antiserum injection. Within a few hours lamellar splitting and vacuolation of myelin began to paranodal regions and Schmidt-Lanterman clefts and there were infiltrating polymorphonuclear cells. By 8 hours without the detectable presence of monocytes or macrophages, myelin vesiculation became advanced and widespread. By 15 hours, endoneurial edema had reached its maximum. Macrophages were found in association with myelinated nerve fibers. From that time through the next 5 days, demyelination progressed to complete denudation of axons by macrophage phagocytosis of myelin. Activated cytoplasm of Schwann cells reinvested demyelinated axons, often in concert with persisting phagocytic macrophages. Peripheral nerve demyelination thus transferred evolved rapidly, and myelin destruction occurred prior to the appearance of monocytes or macrophages. Demyelinating activity was lost after absorption by purified peripheral nerve myelin but not by liver or kidney and was heat-labile and complement dependent (T. Saida, K. Saida, D. H. Silberberg, and M. J. Brown: Nature 272: 639, 1978).
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PMID:Antiserum-mediated demyelination in vivo: a sequential study using intraneural injection of experimental allergic neuritis serum. 73 72

There is evidence that nervous system mast cells may play a role in the pathogenesis of the experimental autoimmune demyelinating diseases, experimental allergic neuritis (EAN), and experimental allergic encephalomyelitis (EAE). We compared mast cell numbers in the peripheral nervous system (PNS) and central nervous system (CNS) of rodent strains that differed in their susceptibility to experimental demyelination. Mast cells were counted by toluidine blue staining of formalin-fixed tissue. Normal Lewis rats (susceptible to both EAN and EAE) had significantly greater numbers of mast cells in the dura mater (about 6x) of the meninges and the sciatic nerve (3x) than Brown Norway rats (resistant to EAE and EAN induction under normal circumstances). Similarly SJL/J mice (susceptible to EAE and EAN) had significantly greater numbers of CNS (3x) and PNS (8x) mast cells than C3H mice (more resistant to disease induction). Other mouse strains were also examined, and PNS mutant Trembler mice had high numbers of PNS mast cells, while the mast cell deficient W/Wv mice contained no detectable mast cells in either the CNS or PNS. Reconstitution of W/Wv mast cells was accomplished by intravenous injection of bone marrow cells from congenic littermates. After seven months, mast cells could be seen in both the CNS and PNS of reconstituted animals. The possibility that mast cells and mast cell precursors can migrate into the nervous system of animals, in the absence of inflammatory disease, may have implications for their role in the pathogenesis of experimental demyelinating diseases.
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PMID:An analysis of mast cell frequency in the rodent nervous system: numbers vary between different strains and can be reconstituted in mast cell-deficient mice. 202 65

T lymphocyte lines specific for the peripheral nerve myelin protein P2 were selected from the lymph nodes of Brown Norway (BN) rats immunized with bovine P2 protein in complete Freund's adjuvant. These T cells expressed the W3/25+, OX8-phenotype and responded specifically to bovine P2 protein, but not to PPD or bovine basic protein, in T cell proliferation assays. When injected i.v. into syngeneic recipients, BN P2-specific T cell lines induced both clinical and histologic signs of experimental allergic neuritis (EAN), overcoming the resistance of this rat strain to actively induced EAN. Although the histopathology of the disease was indistinguishable from that seen in T cell-mediated EAN in the Lewis rat, disease onset was considerably later, 7 to 8 days after cell transfer, as opposed to 4 days in Lewis. This lag phase between inoculation and disease onset could not be further reduced even by raising the cell dose to 50 X 10(6) cells/host. The fine specificity of the T cell response to P2 differs between Lewis- and BN-derived T cell lines. At least one neuritogenic epitope for each strain was present in the cyanogen bromide-derived peptide CB2 (residues 21-113), as shown by the ability of CB2-specific T cell lines derived from each strain to transfer EAN to the appropriate host strain. However, neuritogenic BN T lines fail to mount a response to the sequence 53-78 (SP4), which encompasses an epitope that is neuritogenic for Lewis rats. These results demonstrate that the resistance of BN rats to actively induced EAN is not due to the lack of appropriate P2-specific autoreactive T cell clones in the normal T repertoire. Furthermore, the results suggest that two distinct epitopes of P2 are responsible for EAN in Lewis and BN rats.
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PMID:Induction of experimental allergic neuritis in the BN rat: P2 protein-specific T cells overcome resistance to actively induced disease. 243 Oct 45

Strain differences among rats to the induction and severity of experimental allergic neuritis (EAN) in response to whole PNS myelin were observed. Lewis rats were highly susceptible and developed severe EAN without central nervous system lesions (EAE), while Brown Norway rats were most resistant. Wistar, Sprague-Dawley, and Buffalo rats were susceptible but developed less severe disease than Lewis rats. Only Lewis rats consistantly developed EAN in response to isolated P2 protein. The severity of EAN was enhanced by treatment of the P2 with mercaptoethanol prior to injection. None of the strains developed EAN in response to galactocerebroside and none developed the lesions of EAE in response to any of the bovine myelin antigens tested. Myelin protein profiles from these rat strains were similar which suggests that factors other than target tissue differences, such as genetically determined immune responses to bovine myelin antigens, must be involved in these differing responses.
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PMID:Experimental allergic neuritis. I. Rat strain differences in the response to bovine myelin antigens. 624 43