Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated myelin basic protein (MBP) was less effective than an equivalent amount of spinal cord in inducing protection against experimental allergic encephalomyelitis produced by a challenge of either cord, purified myelin or MBP. Complete protection was only obtained when an MBP challenge was preceded by spinal cord treatment. There was a 100% incidence of disease in the guinea pigs pretreated with MBP before challenge with spinal cord or myelin, but the onset was delayed by 3--4 weeks and the disease was less severe than in the controls. Recurrent disease was seen in some control and pretreated animals challenged with spinal cord but not in animals challenged with MBP.
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PMID:Relative effectiveness of spinal cord and purified myelin basic protein in producing resistance to experimental allergic encephalomyelitis. 8 69

Protection of guinea pigs from experimental allergic encephalomyelitis (EAE) was attempted using bacterial lipopolysaccharide (LPS) from 4 sources. The ability of these LPS to induce DNA synthesis in guinea pig lymph node (LN) cells in vitro was also investigated. It was found that there existed a good correlation between the capacity of LPS to suppress EAE and their degree of mitogenic activities for LN cells. LPS from Escherichia coli 0111:B4 (Ec-LPS), which was most effective in suppressing EAE and also best inducer of DNA synthesis in LN cells, enhanced the proliferation of cells forming antibody to myelin basic protein (BP) in the regional LN. These results, in addition to the previous report, suggested that at the inductive phase the proliferation of B lymphocytes or their products, antibodies to BP, could inhibit formation of T lymphocytes sensitized to BP, resulting in suppression of EAE. Lipid A but not PS fraction of Ec-LPS showed a protective activity against EAE and a mitogenic activity for LN cells although less so than whole LPS. In addition, Lipid A appeared to exert its mitogenic effect mainly on B rather than on T lymphocytes.
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PMID:Correlation between the capacity of bacterial lipopolysaccharide to supress experimental allergic encephalomyelitis and its mitogenic activity for lymph node cells in guinea pigs. 9 30

This study confirms previous reports that myelin basic protein loses its encephalitogenic activity when incubated in normal serum at 37 degrees C. The mechanisms for this was studied. 125I-labelled human myelin basic protein was rapidly degraded by normal guinea pig serum to low molecular weight products as shown by polyacrylamide gel electrophoresis. An intermediate product of molecular weight about 6000 daltons was seen. Plasma had a much lower degradative activity than serum; the half life of myelin basic protein was 3.8 hours in plasma compared with 12 minutes in serum. Serum degraded myelin basic protein was no longer capable of suppressing experimental allergic encephalomyelitis in the guinea pig nor of eliciting delayed-type hypersensitivity in guinea pigs sensitized to myelin basic protein.
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PMID:Studies on the inactivation of encephalitogenic myelin basic protein by serum. 9 76

After intracranial replication of a neurotropic strain of vaccinia in mouse brain, analysis of the purified virus preparation reveals the presence of at least one host protein on the virus which was identified as the myelin basic protein. Vaccinia virus Elstree, a dermotropic virus may substitute for complete Freund's adjuvant (CFA) in inducing experimental allergic encephalomyelitis (EAE). Guinea pigs challenged with virus-myelin emulsions without CFA developed clinical and histological signs of EAE.
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PMID:Mechanisms in the pathogenesis of post-infectious vaccinia virus encephalomyelitis in the mouse. 9 31

Autosensitization to some central nervous system antigen still remains one of the best hypotheses for the continuing pathogenesis of multiple sclerosis (MS). Enough is now known about the cause, pathogenesis, and treatment of experimental allergic encephalomyelitis (EAE) to test this hypothesis. Reports of therapeutic failure of the encephalitogen myelin basic protein (BP) in the treatment of MS have their counterparts in similar therapeutic failures in EAE. Only highly inbred strain 13 guinea pigs respond consistently to BP therapy, and this only when BP is administered in relatively high doses. Noninbred guinea pigs respond much less well to simple BP therapy, and monkeys hardly at all. In both strains of monkeys so far studied, a nonspecific adjunctive factor--an antibiotic in Macaca mulatta and a steroid in Macaca fascicularis--is also required. Accordingly, human trials of the therapeutic efficacy of BP in MS should include its administration in large concentrations together with an adjunctive agent.
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PMID:Has myelin basic protein received a fair trial in the treatment of multiple sclerosis? 9 73

Capacity of basic protein (SCP) to prevent the development of experimental allergic encephalomyelitis was studied in guinea pigs. This protein is shown to possess no antiencephalitogenic effect. Distribution of this protein in various areas of the central and peripheral nervous system was investigated using immune serum to the protein. The protein under study is shown to localize mainly in the peripheral nervous system: spinal roots, sciatic nerve, brachial plexus nerves, vagus and optic nerves, and in the central nervous system areas rich in nerve fibres: spinal cord, medulla oblongata, pons varolii, corpus callosum, white substance of cerebral cortex. The protein content in corpus callosum and white substance of cerebral cortex is extremely insignificant. Using the Ouchterlony reaction of double immunodiffusion the protein under study was found in the myelin membrane of the peripheral nervous system and its immunological identity to the myelin basic protein (P-2) is shown.
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PMID:[Immunological identity of neurospecific (SCP and P-2) proteins and SCP protein distribution in the nervous system]. 9 78

PVG/c rats, infected 3 days previously with 10(3) Trypanosoma brucei brucei S.42 organisms failed to develop adjuvant disease in response to an intradermal inoculation of mycobacterial adjuvant. By contrast, similarly infected rats, immunized with heterologous brain and spinal cord in Freund's complete adjuvant with pertussis vaccine as a secondary adjuvant, developed clinical signs of allergic encephalomyelitis (EAE) at least as severe as those in uninfected rats. Delayed hypersensitivity reactions to PPD were depressed in trypanosome-infected, adjuvant-injected rats, as were the reactions to myelin basic protein in infected rats developing EAE. There appeared to be no cross-reactivity between trypanosomal antigen and myelin basic protein which could account for the lack of suppression of EAE. It is suggested that the different extent to which autoimmunity is involved in these two experimental allergic diseases may account for the differential suppressive activity of trypanosome infections upon them.
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PMID:Differential suppression of experimental allergic diseases in rats infected with trypanosomes. 9 15

New precepts gained from the crescendo of neuroimmunobiologic research of recent decades have increased our understanding of experimental allergic encephalomyelitis (EAE), virus-associated acute disseminated encephalomyelitis (ADE), and multiple sclerosis (MS). EAE of animals and humans provides evidence of the existence in mammalian lymphoid tissues of potential clones of cells with autoreactivity for myelin basic protein (MBP) and other antigenic constituents of the central nervous system (CNS). In a new hamster model, EAE has been strikingly potentiated by persistent infection of the CNS with defective measles virus, a finding that also has implications for virus-associated ADE. Endogenous MBP or MBP degradation fragments, reactive with MBP antibodies of various affinities, have been detected by a recently devised radioimmunoassay in serum, plasma, and other body fluids of normal rats, rats with EAE, and patients with virus-associated ADE or MS. Circulating MBP or MBP fragments may be of great importance in inhibiting neuroautoimmune reactivity and play a role in repair of immunologic CNS injury should it inadvertently occur. Finally, the impressive degree of concordance of immunologic events in EAE, virus-associated ADE, and MS provides additional support for the central importance of host neuroimmunologic responses in the pathogenesis of these neutologic diseases.
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PMID:Joseph E. Smadel Memorial Lecture: neuroimmunologic diseases of animals and humans. 9 35

Treatment with rabbit anti-moneky thymus cell sera whether limited (3 days) or extensive (15 days), did not alter the development of experimental allergic encephalomyelitis (EAE) in rhesus monkeys challenged with myelin basic protein or central nervous system tissue (CNS) when compared to similarly challenged control monkeys treated with normal rabbit serum. No consistent difference in disease incidence or intensity as measured by incubation period, neurologic signs or CNS pathology was observed between experimental and control monkeys. This finding is in contrast to previous reports on the efficacy of ATS treatment in prevention of EAE in rodents.
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PMID:Induction of allergic encephalomyelitis in rhesus monkeys treated with anti monkey thymocyte sera. 11 83

Experimental allergic encephalomyelitis (EAE) was induced in sheep in pursuit of the hypothesis that an immune response against central nervous system antigens might play a role in the pathogenesis of visna. Nine to 12 days after sensitization with whole sheep brain and complete Freund's adjuvant, approximately 50% of sheep developed a fulminating lethal form of EAE. Following a second sensitization, another 20% of animals developed EAE whereas a residual 30% failed to develop any signs or histologic evidence of disease. A histologic comparison of EAE and visna indicated considerable similarity in the nature of the pathologic process. However, the distribution of lesions was quite different, suggesting cellular responses to two different antigens, Cell-mediated immunity to myelin basic protein, as measured by lymphocyte blast transformation, was minimally elevated in sheep sensitized with whole brain suspension in complete Freund's adjuvant, whereas no response could be detected in visna-infected sheep. Complement-fixing antibody titers to basic protein and to a lipid antigen of brain, probably galactocerebroside, rose briskly after sensitization. In visna-infected sheep, on the other hand, there was no increase in either antibody. A large proportion of both Hampshire and Icelandic sheep had low levels of complement-fixing antibody to central nervous system antigens prior to induction of EAE or infection with visna virus. The origin of this antibody is undetermined, but it appeared to have no effect on the course of either disease. Immunosuppression of sheep with antilymphoid serum prevented induction of EAE. Acute EAE was, thus, successfully induced in sheep and used as a model to measure immune responses to central nervous system antigens and as an index of immunosuppression. However, these comparative studies did not provide any evidence for the role of an autoimmune response, to the two central nervous system antigens tested, in the pathogenesis of visna.
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PMID:Pathogenesis of visna. III. Immune responses to central nervous system antigens in experimental allergic encephalomyelitis and visna. 18 62


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