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)

Similarity of the syndromes of rabies and of encephalomyelitis resulting from rabies vaccination poses a problem in differential diagnosis that has had tragic consequences. That difficulty may also be largely responsible for the traditional belief that rabies is inexorably fatal, in that recovery from paralysis is interpreted as evidence that the disease was postvaccinal encephalomyelitis rather than rabies. Diagnosis is additionally complicated by presence of rabies antibodies in serum in both conditions. However, we have found that rabies antibodies elicited by vaccination do not pass the blood/brain barrier to enter the fluids of the CNS in EAE, the experimental counterpart of postvaccinal encephalomyelitis; whereas antibodies are present in high titer as a result of production in situ after recovery from rabies. Therefore a ratio of antibody concentrations of greater than 1:10 in CSF and serum indicates chronic rabies or recovery from that disease.
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PMID:Allergic encephalitis, rabies antibodies, and the blood/brain barrier. 3 89

Colonial bats (Myotis supp. and Eptesicus sp.) were infected with eastern equine encephalomyelitis virus by subcutaneous inoculation or by the bite of infected mosquitoes. Bats were maintained in an environment simulating conditions encountered in hibernacula or in summer maternal colonies. Virus was detected in the blood of hibernating bats at irregular intervals over a 42-day observation period; viremia perhaps was influenced by the amount of disturbance (arousal) involved in the blood sampling process. Target organs included brown fat, spleen, lung, kidneys, pancreas, and liver. Neutralizing antibody was not detected in sera collected from these bats between days 4 and 42 post-inoculation. In nonhibernating bats, virus was recovered from mammary glands, brown fat, pancreas, lungs, kidneys, and liver, in addition to blood. Attempts to infect bats orally or to transmit virus to suckling mice by the bite of viremic bats were unsuccessful. Virus was transmitted from viremic chickens to E. fuscus by the bite of Culiseta melanura and Aedes aegypti.
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PMID:Eastern equine encephalomyelitis virus in experimentally infected bats. 4 Nov 9

6-Chloro-17 alpha-hydroxypregna-1,4,6-triene-3,20-dione (CHP), a steroid having a progestin-type structure yet not having progestational activity, was found to exhibit moderate anti-inflammatory activity in a number of conventional tests for corticoid potency (e.g., thymolytic, granuloma, carrageenin edema). CHP was essentially equipotent, however, with cortisol in models of inflammation mediated via delayed hypersensitivity such as experimental allergic encephalomyelitis, adjuvant-induced arthritis, mouse skin graft, and mouse skin delayed hypersensitivity. In contrast to cortisol, which inhibits both 19-s and 7-s antibody formation, CHP does not diminish the number of cells producing either antibody.
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PMID:A selective inhibitor of the elicitation of immune-mediated reactions. 4 26

A 17-residue peptide (Peptide Y) was isolated from the COOH-terminal end of the basic protein of bovine myelin by peptic digestion. This peptide induced experimental allergic encephalomyelitis in the rhesus monkey. Treatment of Peptide Y with cyanogen bromide released three amino acids from the COOH-terminal end and resulted in a tetradecapeptide (Peptide M) which was also encephalitogenic in the rhesus monkey. The sequence of Peptide M is: Phe-Lys-LEU-Gly-Gly-Arg-Asp-Ser-Arg-Ser-Gly-Ser-Pro-Met. Thus a major disease-inducing site active in the rhesus monkey is contained within a 14-residue peptide localized near the COOH-terminal end of the protein. This peptide differs markedly in location and sequence from the 9-residue peptide shown to contain the encephalitogenic determinant for the guinea pig.
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PMID:Allergic encephalomyelitis. Isolation of an encephalitogenic peptide active in the monkey. 4 30

Defined peptide fragments were isolated from the N-terminal half of the myelin basic protein (BP) molecule and employed for antigen-induced inhibition of experimental allergic encephalomyelitis (EAE). Guinea pigs pretreated with peptide 44-89, obtained by limited pepsin digestion and purified by column chromatography, were significantly protected against EAE subsequently induced by sensitization with BP in complete Fruend's adjuvant. Peptide 1-20, derived by cyanogen bromide cleavage, did not inhibit EAE, nor did the synthetic EAE peptide (residues 114-122), although this peptide was only weakly encephalitogenic for guinea pigs. These findings directly support our previous conclusion that different sites on the BP molecule are responsible for induction and inhibition of EAE, and suggest that disease inhibition can be attributed, at least in part, to a site within peptide 44-89.
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PMID:Antigen-induced inhibition of experimental allergic encephalomyelitis. III. Localization of an inhibitory site distinct from the major encephalitogenic determinant of myelin basic protein. 4 41

After onset of experimental allergic encephalomyelitis (EAE), guinea pigs can be effectively treated by injection with myelin basic protein (BP). In order to localize the site of action of BP, cells from sensitized donors treated with BP one, two, three, or four times after disease onset have been transferred to normal recipients. One injection of BP has no effect on ability of cells to transfer EAE. Two injections partially inhibit transfer. After the third and fourth injections the sensitized cells lose their capacity to transfer EAE. The therapeutic effect of BP previously demonstrated in actively sensitized guinea pigs must involve the specifically sensitized cells rather than the target organ.
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PMID:Adoptive transfer of experimental allergic encephalomyelitis (EAE): prevention of successful transfer by treatment of donors with myelin basic protein. 4 79

After challenge with guiena pig basic protein (GPBP) Lewis (Le) rats, which are homozygous for the immune response experimental allergic encephalomyelitis (Ir-EAE) gene, developed positive delayed skin tests against GPBP and the 43 residue encephalitogenic fragment (EF); in addition, Le rat lymph node cells (LNC) were stimulated and produced migration inhibitory factor (MIF) when incubated in vitro with these antigens. In contrast Brown Norway (BN) rats, which lack the Ir-EAE gene, did not develop delayed skin tests to EF and their LNC were not stimulated and did not produce MIF when incubated in vitro with EF. These observations indicate that the Ir-EAE gene controls a T-cell response against the EF. Le rats produced measurable anti-BP antibody by radioimmunoassay after primary challenge. Although no antibody was detectable in BN rats by radioimmunoassay, radioimmunoelectrophoresis indicated that a small amount of antibody was formed after primary immunization. After boosting intraperitoneally, both strains of rat exhibited a rise in anti-BP antibody; which was greater in Le rats. In both strains of rat the anti-BP antibody reacted with a portion of the molecule other than the EF. Since EF primarily evokes a T cell response, it is suggested that the EF portion of the BP molecule may contain a helper determinant in antibody production.
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PMID:The immune response against myelin basic protein in two strains of rat with different genetic capacity to develop experimental allergic encephalomyelitis. 4 14

Two basic proteins, P1 of molecular weight 14,200 and P2 of molecular weight 12,300, purified from bovine peripheral nerve, were assayed for biological activity. The P1 protein is an exclusively neuritogenic agent, capable of producing clinical signs of experimental allergic neuritis (EAN) and histological abnormalities in the peripheral nervous system (PNS) of guinea pigs and rabbits, without any changes in their central nervous system (CNS). P2 protein, like the CNS basic encephalitogenic protein (BE), has combined neuritogenic and encephalitogenic activities, therefore it induces in these animals neurological signs and pathological evidence of EAN, as well as histological characteristics of experimental allergic encephalomyelitis (EAE).
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PMID:Neuritogenic and encephalitogenic properties of the peripheral nerve basic proteins. 4 20

A canine distemper virus (CDV), DESIGNATED R252, originally recovered from a dog with demyelinating encephalomyelitis was shown to reproduce this disease in gnotobiotic dogs with a high incidence as compared to other CDV strains, which produced an acute fatal infection. In this investigation, R252 was propagated for the first time in Vero cells and compared to two known strains of CDV, Snyder-Hill (SH) and Onderstepoort (Ond). The results of this study revealed that intracellular R252 accumulated more slowly than either SH or Ond. There was extensive destruction of Vero monolayers infected with either R252 or SH. Each virus induced the formation of intracytoplasmic and intranuclear inclusions. Ond infection resulted in minimal cytopathic changes and intracytoplasmic inclusions. Immunofluorescence studies indicated that the spread of R252 infection within the monolayers was intermediate between the rapidly spreading SH and slowly spreading Ond. R252-infected cells developed characteristic immunofluorescent cytoplasmic inclusions. Initially, each stained homogeneously and later appeared as a non fluorescent body surrounded by a fluorescent ring. This characteristic pattern of fluorescence was observed only infrequently in thelate stage of SH infection and was absent in Ond-infected cultures. Reciprocal neutralization studies indicated that the three strains are of one serotype. These findings suggest that R252-CDV has biological properties which differ from two other strains of CDV and which may have bearing upon the in vivo capability of this virus to produce demyelinating encephalomyelitis.
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PMID:Biological properties of a canine distemper virus isolate associated with demyelinating encephalomyelitis. 4 10

Strain 2 guinea pigs develop less severe experimental allergic encephalomyelitis than do strain 13 and Hartley guinea pigs when sensitized with equivalent amounts of homologous myelin basic protein (BP) in complete Freund's adjuvant. In vivo and in vitro correlates of delayed hypersensitivity to myelin basic protein are depressed in the strain 2 guinea pigs relative to the two susceptible strains. The incidence of circulating anti-BP antibodies is also lower in sera from strain 2 guinea pigs than in sera from strain 13 or Hartley guinea pigs. There was no difference among the three strains in their ability to mount delayed hypersensitivity to tuberculin, nor in the response of their cells to PHA in vitro.
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PMID:Experimental allergic encephalomyelitis in resistant and susceptible guinea pigs: in vivo and in vitro correlates. 4 53


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