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)

Lymphocytes from patients with acute transverse myelopathy (ATM) were shown to undergo a specific and significant transformation when cultured in vitro in the presence of either the central nervous myelin basic encephalitogenic protein (BE) or the peripheral nerve myelin P2 protein. A similar pattern of response was demonstrated in acute disseminated encephalomyelitis and in acute myeloradiculitis. Lymphocytes from patients suffering from other autoimmune neurological disorders or other neurological diseases affecting the spinal cord showed no response to there immunologically related antigens, which have previously been found to have the capacity of inducing experimental allergic encephalomyelitis, either alone or with experimental allergic neuritis, when injected into animals. The specific in vitro response to BE and P2 suggests that in vivo sensitization of lymphocytes to such self-antigens occurs in ATM and than a cell-mediated, probably postinfecious autoimmune mechanism may be an important factor in the pathogenesis of the disease.
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PMID:The autoimmune features of acute transverse myelopathy. 7 Oct 13

In studies concerned with the activation of fatty acids, a metabolic step initiating the biosynthesis of fatty acids rendering them suitable for elongation, desaturation, esterification or degradation, we have demonstrated that the activity of acid: Co A ligase (AMP) -- E.C.6.2.1.3. is declined throughout the whole investigated period of experimental allergic encephalomyelitis (EAE). This observation clearly indicates that in this experimental disease it is not only the increased catabolism of lipid constituents furnishing the various membraneous structures, including myelin sheats, but also an overall impaired capacity of synthesing new lipids by the diseased cells of the nervous system which must be taken into consideration.
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PMID:Activity of acid: Co A ligase (AMP) in the course of experimental allergic encephalomyelitis. 7 Dec 44

The encephalitogenic activity of bovine encephalitogenic protein (EP) at at doses from 1 to 33.5 microgram was studied in guinea-pigs. Anencephalitogenicity can be demonstrated at a dose of 1 microgram of EP when given with Freund's complete adjuvant. An increase in the dose of EP results in an increase in encephalitogenicity. Data from a previous paper (Lindh and Bergstrand 1975) supplemented with new data on the encephalitogenic capacity of peptide 89--169 were compared concerning the incidence and strength of experimental allergic encephalomyelitis (EAE) to determine the relative contribution of the various parts of EP to the encephalitogenic properties of the total molecule. Peptide 89--169 shows the same degree of encephalitogenicity as EP, but when the tryptophan residue is blocked (HNB-89-169) the encephalitogenicity is reduced to approx. 15% of the initial amount. Peptide 43--115, tyr (modified at the tyrosine residue 67) appears to have an encephalitogenicity of rather less than 10% of the intact EP molecule, whereas peptide 1--42, if active at all, has an encephalitogenicity of approx. 1% of the total EP molecule. The findings are discussed in the light of a possible cross-reactivity between different determinants of EP.
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PMID:A quantitative study of encephalitogenic protein and peptides in guinea pigs. 7 Dec 46

Several parameters of the in vitro lymphocyte proliferative response to myelin basic protein (BP) in Lewis (Le) and Brown Norway (BN) rats were examined. The results demonstrate that BN rats, a strain normally resistant to BP-induced experimental allergic encephalomyelitis, and Le rats, a strain readily susceptible to the disease, have similar patterns of the proliferative response to BP. An important difference, however, is that BN lymphocytes, although responding significantly to BP, are unable to proliferate to the same level as Le lymphocytes. In experiments measuring the lymphocyte response as a function of antigenic stimulus, days of culture, or type of adjuvant used, the BN rat peak response was in general 70% or less of the Le rat peak response. Furthermore, the BN lymphocyte response was reduced when B cells were removed whereas there was no effect in the Le rat. A negative feedback mechanism, possibly suppressor cells, has been suggested to explain these differences.
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PMID:Kinetics of the in vitro lymphocyte response to myelin basic protein in the the Lewis and Brown Norway strains of rat. 7 6

The activity Na+, K+-ATPase of the guinea pig brain synaptosome fraction as well as the effect on this enzyme of the blood serum obtained in guinea pigs in different periods after sensibilization of the animals with the basic encephalitogenic protein were studied in dynamics of experimental allergic encephalomyelitis development. The Na+,K+-ATPase activity in the guinea pig brain synaptosome fraction is more than 50% lower from the seventh day of sensibilization up to development of characteristic symptoms of the disease in animals. The guinea pigs blood serum obtained on the seventh and tenth days of sensibilization has an inhibitory effect of the same order on the studied activity of the normal guinea pig brain synaptosome fraction. At the later stages of the disease development and with the presence of characteristic symptoms of experimental allergic encephalomyelitis in the animals the blood serum has no similar effect.
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PMID:[Na+-K+-ATPase activity in guinea pig brain synaptosomal fraction in experimental allergic encephalomyelitis]. 7 43

The hemagglutinating antibody responses of Lewis rats with experimental allergic encephalomyelitis (EAE) and of rats rendered unresponsive to this autoimmune disease by pretreatment with myelin basic protein (BP) were compared. Most tolerant animals produced low levels of hemagglutinating antibody. Similarly, most rats with EAE also produced anti-BP antibodies. We were unable to correlate hemagglutinin production or titer with protection against disease. Hemagglutination inhibition (HAI) studies reveal cross-reactivity between rat, guinea pig and bovine BP. HAI studies with BP-derived peptides suggest that at least three distinct antibody-binding determinants exist in the BP molecule, and that individual inbred Lewis rats respond differently with respect to antibody production to these sites.
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PMID:Antibody response to myelin basic protein: comparisons between Lewis rats with experimental allergic encephalomyelitis, and tolerant rats. 7 24

The present study has investigated central nervous system disease in guinea pigs inoculated with emulsions containing purified preparations of bovine oligodendroglia and their fractions isolated with or without trypsinization, whole bovine white matter or myelin basic protein (MBP). The MBP content of the oligodendroglial fractions was determined by radioimmunoassay. It was found that oligodendroglia prepared from trypsinized fresh brain contained minute amounts of MBP and did not induce disease. The corresponding cell fraction from non-trypsinized frozen brain was rich in MBP and induced disease. Bovine white matter and MBP induced typical experimental allergic encephalomyelitis (EAE). The structural preservation of the non-encephalitogenic trypsinized MBP-poor cells was very good and that of the encephalitogenic MBP-rich non-trypsinized cells very poor. It has been concluded that the encephalitogenicity observed was due to MBP, rather than to a specific oligodendroglial antigen.
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PMID:Encephalitogenic properties of purified preparations of bovine oligodendrocytes tested in guinea pigs. 7 47

A woman, aged 26 years, who died of progressively worsening demyelinating encephalomyelitis in the course of 4 years is reported. The neuropathological findings included large subcortical softenings in the cerebral hemispheres, tiny perivenous demyelinated foci in their neighborhood and scattered in the white matter. There was an acute vasculitis with fibrinoid exudation in the affected as well as unaffected areas. Focal perivenous mononuclear cell infiltrations are conspicuous in the white matter. The laboratory and postmortem examinations suggested a collagen disease like SLE. The abnormalities included marked increase of serum gamma-globulin, especially of IgG, and elevation of CRP, RA, and ANA titer, moderate thickening of the basement membranes of the renal glomeruli, onion skin-like periarteriolar fibrosis in the spleen, fibrous pericarditis and periadventitial fibrosis of myocardial arteries. Bilateral degeneration of the spinal posterior columns and dorsal roots was also observed. A probable relationship of the modified features in this example of demyelinating encephalomyelitis with abnormal immune mechanisms in the background is discussed.
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PMID:A case of demyelinating encephalomyelitis with some resemblance to collagen disease. 7 51

The principal pathways by which viruses spread to the central nervous system (C.N.S.) are considered to be direct invasion along peripheral nerves or the haematogenous route. The latter is thought to involve passive transfer or active replication of virus in C.N.S. endothelial cells. In this study histological evidence of mild perivascular encephalomyelitis was found 8-10 days after infection of dogs with canine distemper virus (C.D.V.). C.D.V. antigen and viral nucleocapsids were detectable in the mononuclear cells infiltrating nervous tissue and C.D.V. was isolated from lymphoid tissue and buffy-coat cells. C.N.S. infection may thus be initiated by migrating virus-infected lymphocytes and this pathway may operate in other viral disorders of the C.N.S.
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PMID:Possible initiation of viral encephalomyelitis in dogs by migrating lymphocytes infected with distemper virus. 7 87

The expression of chronic relapsing experimental allergic encephalomyelitis in strain 13 guinea pigs was suppressed with a single series of injections of myelin basic protein in incomplete Freund's adjuvant. The suppression appeared permanent, and subsequent rechallenge with central nervous system antigen failed to elicit exacerbations.
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PMID:Suppression of chronic allergic encephalomyelitis: relevance to multiple sclerosis. 7 24


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