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)

A hyperacute form of experimental autoimmune encephalomyelitis (HEAE) was induced in Lewis rats using small doses (3.2 mug) of guinea pig myelin basic protein as immunogen and B. pertussis vaccine as adjuvant. Myelin basic proteins from species other than guinea pig (rat, man, monkey, pig, ox, rabbit and sheep) induced only ordinary EAE with this adjuvant. HEAE was more readily distinguished from ordinary EAE by clinical criteria (early onset, with a rapid and severe course, and high incidence of cerebral signs and mortality) than by histologic signs which, although characteristic of HEAE. were not pathognomonic for HEAE, HEAE was transferred to x-irradiated syngeneic recipient rats with lymph node cells from appropriately immunized donors. The Brown Norway (BN) strain of rat was found susceptible to induction of ordinary EAE, but not HEAE, using large doses of either rat or guinea pig myelin basic proteins. The unique immunogenicity of the guinea pig basic protein must be due to a different antigenic determinant from the determinant(s) which is shared by rat and guinea pig myelin basic proteins and which without B. pertussis induces ordinary EAE. The adjuvant action of B. pertussis in inducing HEAE in the Lewis rat is most likely mediated through an immunocompetent T lymphocyte.
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PMID:Antigen, host and adjuvant requirements for induction of hyperacute experimental autoimmune encephalomyelitis. 6 74

Bulk-isolated human and bovine oligodendroglia, practically free from myelin, have been used in attempts to elicit an autoimmune response which has been compared with acute experimental allergic encephalomyelitis (EAE). For these experiments, a total of 20 Hartley guinea pigs, 33 Lewis rats and 16 rabbits have been studied. Animals were inoculated with a range of doses of purified preparations of both human and bovine oligodendroglial cells in complete Freund's adjuvant (CFA) and compared with others challenged with whole white matter in CFA. The latter animals all developed clinical and histological signs of experimental allergic encephalomyelitis (EAE) 2-3 weeks post-inoculation. In general, oligodendroglial cells were encephalitogenically less potent than white matter. Guinea pigs were the most susceptible to inoculations of oligodendroglia. In several given human oligodendroglia 14 days earlier, a paraparesis indistinguishable from conventional EAE was seen. Animals receiving bovine cells showed no clinical signs. Histologically, the CNS of afflicted guinea pigs displayed severe inflammation but, in contrast to conventional EAE in the same species, demyelination was rare in the small group of animals tested. After sensitization with oligodendroglia, rats displayed no clinical disease. Histologically, some given human cells had positive evidence of disease while bovine cells in others gave a mild response. Rabbits showed no clinical and very little histological disease. Although more extensive studies are needed to confirm the findings, from the animals studied it appears that (1) variation in response to inocula containing oligodendroglia exists among the species tested, (2) that human oligodendroglia are more potent immunologically than bovine cells, (3) that CNS lesions produced by these cells in guinea pigs, lack a strong demyelinative component and (4) a specific antigen might exist in oligodendrocytes which is distinct from myelin basic protein. The possible reasons underlying our findings are discussed.
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PMID:Studies on the encephalitogenic effects of purified preparations of human and bovine oligodendrocytes. 6 80

In order to elucidate the role of humoral antibodies in the pathogenesis of myelin lesions in experimental allergic encephalomyelitis (EAE) a combined in vivo and in vitro study was done using rabbits immunized with the purified A1 basic protein. Rabbits injected with whole white matter were used for comparison. Demyelinating activity appeared in the rabbit sera 5 days after injection, as tested in myelinated organotypic tissue cultures. In spite of this no lesions of the myelin preceded the appearance of inflammatory cells in the living animals. In the spinal cord changes in vascular permeability, as revealed by leakage of Evans blue-albumin complex, appeared at the same time as the cells. In contrast to in vitro, the mere presence of circulating antibodies in vivo does not appear to be enough to cause structural changes of the myelin. Possible reasons for this discrepancy are discussed; it is emphasized that the inflammatory changes develope first in areas where the so-called blood-brain barrier to diffusion of proteins is lacking.
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PMID:About demyelinating properties of humoral antibodies in experimental allergic encephalomyelitis. In vivo and in vitro studies. 6

Two peptic fragments (residues 37-88 and 43-88) of guinea pig myelin basic protein which are capable of inducing experimental allergic encephalomyelitis in Lewis rats were cleaved to shorter fragments with alpha-protease (Crotalus atrox proteinase, EC 3.4.24.1) and thermolysin (EC 3.4.24.4). The fragments were isolated, purified, and identified by amino acid composition and NH2- and COOH-terminal residues. The time courses of the reactions, monitored by thin layer electrophoresis of the digests, showed that alpha-protease cleaves peptide (43-88) initially at the Pro(71)-Gln(72) bond, and that the product peptides are subsequently attacked at the Arg(63) -Thr(64), Ser(74)-Gln(75), Arg(78)-Ser(79), and Ser(76)-Gln(80) bonds. No significant cleavages occurred at the -Leu, -Val, and -Ala bonds. These results are in striking contrast to those obtained previously by others workers with other peptide substrates, where selective cleavage at hydrophobic residues occurred. Thermolysin was found to attack peptide (37-88) at the Phe(42)-Phe(43) bond very rapidly; the product peptides were subsequently attacked at the His(60)-Ala(61), Ser(38)-Ile(39)-Tyr(67)-Gly(68), and Pro(84)-Val(85) bonds. These cleavages are compatible with the known specificity of this enzyme. Several of the fragments prepared with these two enzymes, peptides (43-71), (61-88), (75-88), and (72-84) have been used in other studies to locate the encephalitogenic site in the parent peptic peptide.
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PMID:Treatment of an encephalitogenic peptide from guinea pig myelin basic protein with alpha-protease and thermolysin. Isolation of fragments and determination of cleavage sites. 6 52

Hemagglutinating encephalomyelitis virus of swine (HEV) was adapted to growth in suckling mouse brain. Electron micrographs of HEV-infected suckling mouse brain, prepared by negative staining and thin-section techniques, exhibited typical morphological characteristics shared with other members of the Coronaviridae. The adaptation of HEV to suckling mouse brain facilitated serologic testing by the use of common host reagents and compatible animal systems. With hemagglutination inhibition, complement-fixation, and neutralization tests, an antigenic relationship was demonstrated between human coronavirus OC 43 and HEV in specific immune and hyperimmune animal sera. Children and adults with seroconversion to OC 43 antigen had diagnostic rises in titer of antibody to HEV antigens. Individuals with seroconversion to human coronaviruse 229E and B814 demonstrated antibody to HEV but not diagnostic rises in titer. Swine with titers of antibody to HEV had lower or no detectable titers of antibody to coronavirus OC 43. Although the prevalence and geometric mean titer of antibody to OC 43 were higher than the titer of antibody to HEV in every group of normal humans tested, significant differences in antibody response to coronavirus OC 43 and HEV were seen between populations that did or did not have possible contact with swine. The evidence suggested that antibody to HEV in humans probably represented a heterologous response to infection with coronavirus OC 43. However, a heterotypic response to unknown or uncharacterized strains of coronavirus cannot be excluded.
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PMID:Antigenic relationship between human coronavirus strain OC 43 and hemagglutinating encephalomyelitis virus strain 67N of swine: antibody responses in human and animal sera. 6 39

Two amino acid sequences from the same regions of guinea pig and bovine myelin basic protein which induce experimental allergic encephalomyelitis in Lewis rats were synthesized. The sequences of these two regions may be defined by residues 69 to 84 of the bovine basic protein. The encephalitogenic sequence from guinea pig basic protein (peptide S49), H-Gly-Ser-Leu-Pro-Gln-Lys-Ala-Gin-Arg-Pro-Gin-Asp-Glu-Asn-OH, is a much more potent encephalitogen than that of H-Gly-Ser-Leu-Pro-Gln-Lys-Ala-Gln-Gly-His-Arg-Pro-Gln-Asp-Glu-Asn-OH (peptide S8) found in the bovine protein. The primary structures of the two determinants are similar; however, a Gly-His deletion from the guinea pig sequence is noted. Study of the encephalitogenicity of peptide S49, peptide S8, and the parent proteins suggests that the difference in the encephalitogenic potency of the parent proteins in Lewis rats is due to a natural modification in the primary structure of their respective encephalitogenic determinants.
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PMID:Experimental allergic encephalomyelitis in Lewis rats: chemical synthesis of disease-inducing determinant. 6 39

Lewis and PVG strains of rats and their F1-hybrids were challenged with guinea-pig or bovine encephalitogenic protein (EP) in Freund's complete adjuvant (FCA) to produce experimental allergic encephalomyelitis (EAE). The Lewis and F1-rats were also challenged with guinea-pig EP in FCA with a fivefold lower concentration of Mycobacterium butyricum. Data are presented concerning clinical signs and histological changes of EAE showing an intermediate position of susceptibility to EAE for the F1-hybrids compared to the parental strains. The findings are discussed in relation to the mode of inheritance of susceptibility to EAE. Among rats immunized with bovine encephalitogenic protein in FCA a weak activity was registered; this was difficult to evaluate, as it could be an effect of FCA only.
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PMID:Susceptibility to experimental allergic encephalomyelitis in two strains of rats and their hybrids. 6 42

The effect on encephalitogenicity of using a serinyl substitution for the glutaminyl group in the peptide ser arg phe ser trp gly ala glu gly gln arg is reported. We conclude from these results that the function of the glutaminyl residue is assisting this peptide to produce allergic encephalomyelitis in guinea pigs is as a hydrogen donor-receptor.
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PMID:Further definition of the encephalitogenic region for guinea pigs. 6 93

Conjugates of myelin encephalitogenic basic protein (EP) and commercial horseradish peroxidase (HRP) have been used for immunohistochemical demonstrations of anti-EP antibody in animals with experimental allergic encephalomyelitis. We performed gel electrophoresis studies on EP-HRP conjugates prepared with glutaraldehyde and on mixtures of EP and HRP incubated without glutaraldehyde. The results show that under conditions of one-and two-step coupling HRP causes rapid loss of the native EP band, apparently due to EP degradation. The EP-HRP mixtures are not encephalitogenic in rabbits, or encephalitogenic activity is lost during processing. The immunohistochemical reactivity of conjugates, however, signals some preservation of antibody-combining sites. The mechanism of the HRP effect on EP is unknown. The possibilities of a contaminating proteinase or direct peroxidatic attack are suggested. Until this action of HRP can be overcome, the effect of coupling procedures on the biological activities of EP will be difficult to assess, and EP-HRP conjugates cannot be expected to reveal sites that may bind encephalitogenic portions of the EP molecule.
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PMID:Commercial horseradish peroxidase degrades myelin encephalitogenic protein during coupling for immunohistochemical studies. 6 67

We determined requirements for the induction of immunoregulatory suppressor cells in experimental allergic encephalomyelitis (EAE) in Lewis rats. Pretreatment of rats with myelin basic protein (BP) in incomplete Freund's adjuvant (IFA) stimulates the proliferation of suppressor cells that localize in lymph nodes and spleen (but not thymus) and exert control over the development of clinical EAE. Dosage studies revealed that 3 X 10(7) suppressor cells can adoptively transfer suppression to syngeneic recipients. Transferred unresponsiveness wanes within 3 weeks, indicating that the suppressor cells are short-lived lymphocytes, although actively induced unresponsiveness persists for at least 8 weeks, probably as a result of continual proliferation under the influence of antigen. No evidence was obtained to suggest that antigen carry-over or blocking antibody production accounts for adoptive transfer of unresponsiveness. Suppressor cells apparently act at the inductive phase of the immune response since they had no inhibitory effect on adoptive transfer of disease by effector lymph node cells. Other mechanisms also may play a role in unresponsiveness to EAE, since rats pretreated i.v. with high dosages of soluble BP were temporarily rendered unresponsive, although suppressor cells could not be detected in these animals.
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PMID:Immunoregulation of experimental allergic encephalomyelitis: conditions for induction of suppressor cells and analysis of mechanism. 7 Apr 89


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