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)

Experimental allergic encephalomyelitis has been induced in guinea pigs using the encephalitogenic tryptophan peptide as antigen and a hydrosoluble adjuvant extracted from Mycobacterium tuberculosis, var. hominis, strain H37Ra. The maximum response was observed using 100mug of adjuvant per animal. This is a quantity of adjuvant substantially higher than was necessary to induce disease utilizing the whole myelin basic protein as antigen.
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PMID:Induction of allergic encephalomyelitis using hydrosoluble adjuvant and the tryptophan region of myelin basic protein. 5 9

The administration of synthetic peptide S42 leads to suppression and reversal of experimental allergic encephalomyelitis (EAE) induced in guinea pigs by myelin basic protein. Peptide S42 contains a linear sequence of 21 amino acid residues, H-Phe-Ser-Trp-Gln-Lys-Phe-Ser-Trp-Gln-Lys-Phe-Ser-Trp-Gln-Lys-Phe-Ser-Trp-Gln-Lys-Gly-OH, made up of four repeating unit sequences of H-Phe-Ser-Trp-Gln-Lys-OH in addition to a C-terminal glycine. Injected at relatively high doses, peptide S42 is non-encephalitogenic. It induces delayed-type hypersensitivity which is not followed by EAE, and elicits delayed-type hypersensitivity responses in peptide S42, encephalitogenic trytophan peptide, or BP-challenged animals for either of the three antigens. The repeating unit sequence of peptide S42 is analogous to the encephalitogenic tryptophan region of the BP molecules . The sequence homology is responsible for cellular recognition of this antigen by the skin test assay and suggests in vivo interaction between peptide S42 and EAE-inducing cells leading to suppression and reversal of disease.
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PMID:Suppression and reversal of allergic encephalomyelitis in guinea pigs with a non-encephalitogenic analogue of the tryptophan region of the myelin basic protein. 5 84

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

This brief report develops the ideas of some previous works underlying a possible functional disequilibrium of tryptophan metabolism in patients affected by Multiple Sclerosis (M.S.) and in animals with experimental allergic encephalomyelitis. So, the urinary excretion of one of the terminal metabolites of the kynurenine pathway of tryptophan, the N1-Methylnicotinamide has been confronted in M.S. patients and in healthy volunteers, in order to put in evidence a possible alteration of the same in M.S. patients. The A.A. could not find any significant difference of the N1-Methylnicotinamide urinary output between controls and M.S. patients; afterwards they have critically revised this result.
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PMID:N1-Methylnicotinamide urinary output in multiple sclerosis affected patients. 14 15

Catecholamine and indoleamine neurotransmitters, together with some of their precursors and metabolites, were determined using HPLC in three brain and two spinal cord regions of Lewis rats with chronic relapsing allergic encephalomyelitis and of control rats injected with complete Freund's adjuvant. Three attacks and two recovery phases were investigated. Changes are found mainly in the spinal cord. In the lumbosacral region both 5-hydroxytryptamine and noradrenaline are reduced during the entire course of the disease, whereas in the craniothoracal region 5-hydroxytryptamine is unchanged and only noradrenaline is reduced during the attacks, returning to normal during the first recovery. The precursors tyrosine and tryptophan are greatly elevated during the first two attacks in both regions. The 5-hydroxytryptamine turnover marker 5-hydroxyindoleacetic acid is increased in the first attack in both regions, then it decreases in the later stages, indicating destruction of nerve fibers. On the fourth and seventh days after inoculation values are generally not significantly different from controls in all regions. The possible correlation of neurochemical results with neurological signs is discussed.
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PMID:Changes of neurotransmitter systems in chronic relapsing experimental allergic encephalomyelitis in rat brain and spinal cord. 242 58

A major disease-inducing site for induction of experimental allergic encephalomyelitis in monkeys exists in Peptide P 14, the 37-residue segment of the A1 protein comprising its COOH-terminus. The peptide appears to contain the dominant encephalitogenic determinant, since it was as active as the A1 protein on a molar basis. By contrast, the 9-residue tryptophan region and the Peptide R region, active in guinea pigs and rabbits, respectively, were comparatively inactive in monkeys. The clinical and histologic expression of the disease produced by Peptide P 14 appeared identical to that induced by the intact A1 protein.
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PMID:Allergic encephalomyelitis in monkeys induced by a peptide from the A1 protein. 411 Oct 48

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease of the central nervous system (CNS). Studies have shown that the encephalitogen responsible for EAE is the basic protein (BP) found inCNS myelin and is, perhaps, the only encephalitogenic component of the CNS. Purified lipophilin, a hydrophobic lipoprotein of myelin, was tested for its ability to induce EAE in guinea pigs. Animals challenged with myelin lipophilin (in CFA) developed clinical and histological signs of EAE which were indistinguishable from those developed by animals challenged with myelin BP (in CFA). Both lipophilin and BP induced and elicited delayed type hypersensitivity in animals challenged with either antigen and the development of delayed type hypersensitivity correlated with eventual onset of clinical signs of disease. The absence of BP from the lipophilin preparation used in this study was documented by several purification procedures and chemical modification of tryptophan in lipophilin, destroyed its ability to induce EAE. These results demonstrate that myelin lipophilin is encephalitogenic and induces a cell-mediated immune disease of the CNS similar, if not identical, to BP-induced EAE. Tryptophan, which is known to be an essential residue in the BP-determinant for disease in guinea pigs, is required for the encephalitogenic activity of lipophilin.
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PMID:Myelin lipophilin-induced experimental allergic encephalomyelitis in guinea pigs. 615 58

Guinea pigs can be rendered unresponsive to experimental allergic encephalomyelitis (EAE) challenge by prior injections of myelin basic protein (BP) or peptides derived from BP. The synthesized tryptophan-containing peptide (TrpP, corresponding to residues 114-122) which is the primary encephalitogenic sequence in BP (for guinea pigs) had been conjugated to the non-central nervous system protein bovine serum albumin (BSA) and used for EAE challenge. It has been shown in this study that prechallenge treatment with the BSA carrier alone can significantly inhibit the induction of EAE by TrpP-BSA conjugate. That carrier treatment is immunologically specific was determined when prior treatment with cytochrome c did not protect animals from EAE challenge with TrpP conjugated to BSA. In addition, in disease induced with BP or TrpP, and while TrpP did protect guinea pigs challenged with TrpP, it did not protect those challenged with BP. This last finding raises the possibility of a second encephalitogenic sequence in BP or an important role for the carrier in the TrpP conjugate.
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PMID:Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide-carrier conjugate. 616 82

Serotonin mediated bulbospinal motor activities were examined in rats with experimental allergic encephalomyelitis (EAE)-induced-paraplegia. Treatment with monoamine oxidase inhibitors and L-tryptophan failed to elicit the components of the serotonin syndrome which involved levels of the neuraxis manifesting flaccid paralysis. Straub tail, hindlimb abduction and hindlimb rigidity did not occur. The motor responses represented at spinal segments just above the level of paraplegia, lateral head weaving and forepaw treading, were present but altered in the diseased rats. No impairment was evident in the production of head tremor or hyper-reactivity to accoustic and tactile stimuli. Similarly, in urethane-anesthetized EAE rats, serotonergically-evoked automatic swallowing activity was unchanged as judged by the effects of serotonin receptor agonists, and a serotonin precursor, a reuptake blocker and an antagonist. Our data support the conclusion that EAE-induced impairment of serotonergic neurotransmission is correlated with motor deficits manfested during the acute paralytic stage of the disease.
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PMID:Central serotonin receptor sensitivity in rats with experimental allergic encephalomyelitis. 696 16

Previously, six T cell clones, which are specific for an encephalitogenic determinant of myelin proteolipid protein (PLP) peptide residues 139 to 151 (HSLGKWLGHPDKF), were derived from SJL mice and shown to use diverse TCR genes. To design TCR antagonist peptides that could interfere with the activation of these clones in vitro and inhibit experimental allergic encephalomyelitis (EAE) in vivo, we first determined the TCR and MHC contact residues of the encephalitogenic peptide. The analysis indicated that residues 144 (tryptophan) and 147 (histidine) were the TCR binding sites and that residues 145 (leucine) and 148 (proline) were important for MHC class II (IAs) binding. On the basis of this information, a peptide analogue (leucine 144/arginine 147), in which both of the major TCR contact residues were substituted, was synthesized. This analogue acts as a TCR antagonist for the panel of PLP 139-151-specific T cell clones, does not cause EAE by itself, blocks the induction of disease by the native 139-151 peptide, and prevents clinical disease progression if administered at the first signs of disease. Thus, although multiple TCR genes are used by PLP 139-151-specific clones, a single peptide analogue can interfere with the disease process. This approach should be feasible for designing peptide analogues that can be tested for therapeutic efficacy in human autoimmune diseases in which the pathogenic Ags are known and TCR use is diverse.
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PMID:A single TCR antagonist peptide inhibits experimental allergic encephalomyelitis mediated by a diverse T cell repertoire. 752 58


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