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 (EAE) was induced in rats of various genotypes by injection of 10 microg guinea pig basic protein in complete Freund's adjuvant containing 100 microg H(37) RV M. tuberculosis. Histologically verified EAE was present in 20/20 Lewis, 17/17 (Lewis x BN)F(1), 9/9 Lewis backcross, and 21/42 BN backcross rats. Among the BN backcross animals, 25/42 were determined to carry the major histocompatibility type characteristic of the Lewis strain and 21 of these had EAE. Separate groups of Lewis, BN, and (Lewis x BN)F(1) rats were immunized as described and skin tested on day 13 with 10 microg guinea pig basic protein and rat S basic protein. Animals of each genotype had Arthus and delayed skin reactivity to both antigens. These data are compatible with the hypothesis that susceptibility to EAE in rats is controlled by an autosomal dominant gene linked to the major histocompatibility locus. It is proposed that this is an immune response gene, designated Ir-EAE, which controls T cell reactivity directed against a highly encephalitogenic portion of the basic protein molecule.
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PMID:Linkage of susceptibility to experimental allergic encephalomyelitis to the major histocompatibility locus in the rat. 412 46

Protection against experimental allergic encephalomyelitis (EAE) was examined by prior injection of following materials with Freund's incomplete adjuvant (FIA), Mycobacterium tuberculosis (Tbc), synthetic muramyl dipeptide (Mdp), polyinosinate-polycytidylate (poly IC), or myelin basic protein (BP). 26 days later, guinea pigs received encephalitogenic challenge in the form of 20 micrograms BP + 20 micrograms Tbc in FIA (BP + Tbc) or 20 micrograms BP + 10 micrograms Mdp in FIA (BP + Mdp). (1) Either pretreatment with Mdp, poly IC or FIA alone showed no protecting effects. (2) Tbc/FIA was not effective on challenge with BP + Mdp, but effective on challenge with BP + Tbc, and produced passive hemagglutinating (PH) antibodies of moderate titer and and complement fixing (CF) antibodies of higher titer. (3) BP/FIA was effective on both BP + Tbc and BP + Mdp challenges, and produced PH antibodies of higher titer than that of CF antibodies. (4) Clinicopathological survey revealed that the challenge with BP + Mdp was blocked perfectly by prior injection with BP/FIA whereas the challenge with BP + Tbc was incompletely blocked by either Tbc/FIA or BP/FIA pretreatment. (5) The finding was verified also by cerebrospinal fluid cell count at the termination of clinical observation. As compared with FCA, Mdp adjuvant itself has no antigenic component, which seems to explain the results in this study.
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PMID:Pretreatment with antigen or adjuvant, and the preventability of allergic encephalomyelitis induced by basic protein with synthetic muramyl dipeptide in comparison with Freund's complete adjuvant. 608 88

Experimental allergic encephalomyelitis (EAE) was induced in guinea pigs with bovine myelin basic protein (BP) with adjuvant of either synthetic muramyl dipeptide (Mdp) or Mycobacterium tuberculosis (Tbc). The following results were obtained: (1) The body temperature of the animals was studied serially after sensitization and its elevation was shown to be an early sign of EAE. (2) Several animals developed the clinical and histological signs of hyperacute EAE. (3) An optimal combined dosage of BP and adjuvant was found for induction of clinical EAE and for the the production of complement fixing (CF) antibodies. (4) Little passive hemagglutinating (PH) antibody was produced by single immunization. These results displayed no essential difference in EAE induced by either adjuvant. (5) Detectable PH antibodies developed later in addition to CF antibodies in a few animals immunized with Tbc adjuvant. These animals were skin-tested to BP, and had recovered from body weight loss or limb weakness. The results suggest that humoral antibodies play a role in modifying the disease process, even if they are not essential in production of EAE.
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PMID:Experimental allergic encephalomyelitis induced by basic protein with synthetic adjuvant in comparison with Freund's complete adjuvant. Role of antibodies in correlation with the clinicopathological features. 617 Jul 38

Experimental allergic encephalomyelitis (EAE) is a disease produced by inoculation of myelin basic protein (BP) into susceptible animals. Data in this report link the production of anti-BP antibody to the murine H-2 histocompatibility background. H-2k and H-2a animals produce high levels of anti-BP antibodies as measuring during both primary and secondary immune responses. Strains with H-2b,d,p,q,s haplotypes are poor responders after primary immunization; however some H-2s and H-2d animals showed an increase in antibody after boosting. The use of M. tuberculosis instead of M. butyricum resulted in greater antibody production in H-2d strains. The response observed in 4 congenic pairs of mice support the association between antibody formation and the H-2 complex. Experiments with recombination inbred strains indicate that responsible genes reside in the I-A region of the H-2 complex.
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PMID:Genetic control of antibody production to myelin basic protein in mice. 617 96

SJL/J, PL/J, and (SJL/J x PL/J)F1 mice were immunized with bovine, guinea pig, mouse, or rat myelin basic proteins (MBP) in adjuvant containing Mycobacterium tuberculosis H37Ra. Twenty-four and 72 hr later, Bordetella pertussis vaccine was given i.v. All MBP tested induced experimental allergic encephalomyelitis (EAE) in SJL/J and F1 mice; however, bovine MBP was inactive in PL/J mice. Each strain was immunized in a similar manner with peptic peptides, residues 1-37, 43-88, and 89-169 of guinea pig MBP. In contrast to the SJL/J strain, which has been shown to recognize a major encephalitogenic determinant in peptide 89-169, PL/J and F1 mice responded primarily to an encephalitogenic determinant within peptide 1-37. Analysis of antibody levels showed that SJL/J mice made no antibody to peptide 1-37, although anti-peptide 89-169 antibodies were consistently found. Conversely, PL/J mice responded well to peptide 1-37, but only an occasional animal made a significant response to peptide 89-169. (SJL/J x PL/J)F1 mice were more susceptible to EAE than either parental strain, as shown by the percentage of animals showing neurologic signs and by clinical severity.
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PMID:Induction of experimental allergic encephalomyelitis in PL/J and (SJL/J x PL/J)F1 mice by myelin basic protein and its peptides: localization of a second encephalitogenic determinant. 618 47

During chronic relapsing experimental allergic encephalomyelitis (r-EAE) in guinea pigs, serum IgM and IgG concentrations increased markedly early in disease. Serum IgM and IgG increased similarly in control animals immunized with Freund's incomplete adjuvant (FIA) and Mycobacterium tuberculosis (MT). In the chronic phase of r-EAE but not in control animals, elevated IgM was also found in central nervous system (CNS) extracts, suggesting intrathecal IgM synthesis. IgG antibodies against myelin and myelin basic protein (MBP) were regularly detected in r-EAE sera from day 21 post inoculation (p.i.), reaching maximum levels in the early chronic phase. IgG antibodies against galactocerebroside (GC) and galactose appeared in some r-EAE sera. Oligoclonal IgG bands were demonstrated in all r-EAE guinea pig sera 21-26 days p.i. The bands in serum decreased in number and strength in the chronic phase. They could be traced to antibodies against MT in 4 of 10 animals, but not to antibodies against myelin, MBP, GC or galactose. Oligoclonal IgG bands were also regularly visualized in r-EAE CNS 124 days p.i., suggesting persistent intrathecal IgG synthesis. They varied in number and migration between different regions of individual CNS. Oligoclonal CNS IgG was related to antibodies against MT in only one of 7 animals, and in no case to antibodies against myelin.
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PMID:IgM and IgG responses during chronic relapsing experimental allergic encephalomyelitis (r-EAE). 620 34

Lines of rat T lymphocytes responsive to the basic protein of myelin (BP) or to the purified protein derivative of Mycobacterium tuberculosis (PPD) were inoculated i.v. into recipient rats. As reported previously, the anti-BP line cells, but not the anti-PPD line cells spontaneously accumulated in the central nervous system and caused encephalomyelitis. However, the anti-PPD line cells could be induced to enter the brain and cause bystander encephalitis by intracerebral inoculation of PPD. Anti-PPD or anti-BP line cells could mediate delayed-type hypersensitivity skin reactions or bystander arthritis elicited by specific antigen. The lines did not cause specific cytolysis in vitro. Susceptibility to delayed-type hypersensitivity or bystander disease was long lasting in rats inoculated with anti-PPD line cells, while rats inoculated with anti-BP line cells were susceptible for only a few days. Thus, lines of T lymphocytes can mediate a variety of pathological reactions directed by the presence of specific antigen, self or foreign.
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PMID:T lymphocyte lines induce autoimmune encephalomyelitis, delayed hypersensitivity and bystander encephalitis or arthritis. 620 82

Pretreatment of Tuck Wistar rats with cyclophosphamide (100 mg kg-1) intraperitoneally prevents the development of adjuvant-induced arthritis, experimental allergic encephalomyelitis and the delayed skin reactions after ovalbumin and Freund's incomplete adjuvant. The resistance of these rats to these stimuli is similar to that found in untreated NR Wistar rats which are resistant to dextran. However, cyclophosphamide suppresses the responses of Tuck Wistar rats to collagen-induced arthritis and sheep red blood cell agglutination, stimuli to which untreated NR Wistar rats respond. Nevertheless, the reactions of Tuck animals to the purified protein derivative of M. tuberculosis, the skin sensitisation to oxazolone, and the development of the delayed reaction after ovalbumin and Freund's complete adjuvant remain unchanged after cyclophosphamide pretreatment. The results indicate the possible existence of two separate types of delayed hypersensitivity reactions.
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PMID:The effects of cyclophosphamide on delayed hypersensitivity in rats. 622 92

Pertussigen, one of the biologically active proteins from Bordetella pertussis, was found highly active as an adjuvant to promote the induction of experimental allergic encephalomyelitis (EAE) in (SJL X BALB/c)F1 mice that had received at the same time an injection of mouse spinal cord (MSC) homogenized in complete Freund's adjuvant containing 4 mg of Mycobacterium tuberculosis H37RA per milliliter (CFA-H37). In this system 2 mg of MSC induced EAE, but a dose of 4 mg was more effective. As little as 250 ng of pertussigen facilitated induction of EAE, and 400 ng uniformly did so. Pertussigen was most effective when given iv from 1 day before to 5 days after administration of MSC homogenized in CFA-H37, when a uniform and severe disease was induced 11-13 days after immunization. Pertussigen given as late as 20 days after MSC-CFA-H37 still precipitated a mild form of EAE which appeared 8-12 days after the injection of pertussigen. When pertussigen was given 5 days after immunization, a chronic, nonfatal type of EAE was induced, and this persisted for the entire 74 days of observation. Histologic findings in the brain and spinal cord 15 days after sensitization in mice which received pertussigen and developed EAE showed perivascular infiltrates consisting mainly of mononuclear cells.
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PMID:Elicitation of experimental allergic encephalomyelitis (EAE) in mice with the aid of pertussigen. 660 26

A single injection dose-response curve was done in the SJL/J mouse using varying amounts of syngeneic spinal cord homogenate and Mycobacterium tuberculosis H37RA in a Freund's type of adjuvant. Inoculation with as little as 0.025 mg. of cord homogenate induced severe experimental allergic encephalomyelitis in some mice. Possible reasons for the great ease of induction of experimental allergic encephalomyelitis with this single injection regimen in comparison with other single injection schemes are discussed. No single injection dose combination was found that induced severe experimental allergic encephalomyelitis in all of a group of mice. When two injections 1 week apart were given, all mice so injected developed severe experimental allergic encephalomyelitis, all had relapses, and nine of 10 had multiple relapses. The number of relapses and severity of residual neurologic deficits were much greater in the two-injection group than in the single injection group.
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PMID:Relapsing experimental allergic encephalomyelitis in the SJL/J mouse. 679 24


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