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)

Strains of mice (BALB/c An Bradley/Wehi, C57B1/10J, CBA/ca H Wehi, DBA/2 Wf, A/J Wehi), thought to be genetically resistant to experimental allergic encephalomyelitis (EAE) and known to be resistant to becoming hypersensitive to histamine after administration of pertussis vaccine were tested for their ability to develop EAE when purified pertussigen was included in the immunization. It was found that C57B1/10J, CBA/ca H Wehi, BALB/c An Bradley/Wehi and DBA/2 Wf developed typical signs and histologic evidence of EAE. The A/J Wehi and the B10D2/n Sn (not previously tested) strains developed only mild signs of EAE, while the known susceptible (SJL/J X BALB/c An Bradley/Wehi) F1 hybrids developed severe EAE. Histologic evidence of EAE was lacking in A/J Wehi mice and was minimal in B10D2/n Sn mice. These results suggest that neither the H-2 complex nor the gene controlling susceptibility to sensitization to histamine by administration of pertussigen are wholly responsible for susceptibility to EAE.
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PMID:Production of experimental allergic encephalomyelitis with the aid of pertussigen in mouse strains considered genetically resistant. 654 69

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

The sensitization of guinea-pigs with the mixture of meningococci and heterologous-cerebral tissue commonly induces the development of the typical clinical and pathomorphological picture of allergic encephalomyelitis. Unlike Mycobacterium tuberculosis and other acid-resistant bacterial and much like Bordetella pertussis, meningococci are capable of inducing allergic encephalomyelitis when introduced in mixture with oil without cerebral tissue. The vaccinal strain induces allergic encephalomyelitis with a more moderate course of the disease.
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PMID:[Experimental allergic encephalomyelitis in guinea pigs caused by meningococci]. 680 Jan 62

The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2s and H-2q, respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2s or H-2q strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (KsIsD?) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate responder H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 hapotype and histamine sensitivity is required for the development of acute EAE.
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PMID:Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes. 680 29

The neuropathology has been described of chronic, relapsing experimental allergic encephalomyelitis produced in SJL/J mice given two injections of isogeneic spinal cord in complete Freund's adjuvant, 1 week apart. The inducing inoculum contained no Bordetella pertussis. The central nervous system changes included hemorrhagic lesions and significant nerve fiber depletion during the early stages of disease, demyelination followed by remyelination, influxes of polymorphonuclear leukocytes and hemorrhage with each acute episode, extensive gliosis, and some Schwann cell invasion and myelination within the central nervous system. Since the mouse is a highly accessible species that is immunologically well understood, this model might lend itself to fuller dissection of autoimmune events associated with recurrent demyelination, problems of considerable significance to multiple sclerosis research.
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PMID:Chronologic neuropathology of relapsing experimental allergic encephalomyelitis in the mouse. 706 21

The effect was studied of varying the dosage of mycobacteria and pertussis vaccine in the immunization emulsion on the development of delayed, relapsing experimental allergic encephalomyelitis (DR-EAE) in SJL/J mice. DR-EAE could be induced with dosages of mycobacteria from 0.2 mg to 1.0 mg per mouse. Animals given pertussis vaccine from different batches and different sources all developed DR-EAE with similar percentages of animals sick, animals relapsing, and delay to onset. Mice immunized without pertussis vaccine also developed DR-EAE but had fewer relapses and a longer delay to onset. The role of antigens and adjuvants in relapsing EAE and analogies with multiple sclerosis are discussed.
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PMID:Delayed, relapsing experimental allergic encephalomyelitis in mice. Role of adjuvants and pertussis vaccine. 715 81

Ten inbred strains of mice were tested for their susceptibility to experimental allergic encephalomyelitis (EAE) after sensitization with mouse spinal cord in complete Freund's adjuvant followed by booster injections of Bordetella pertussis. The results extended previous findings in that not all susceptible mice possessed the H-2s haplotype, but mice with an H-2q background (DBA1/J strain) were also susceptible. Neuropathologic examination of experimental allergic encephalomyelitis in the mouse showed that from strain to strain, the condition was similar. The over-all pathologic picture was somewhat midway between that seen in other species sensitized with whole nervous tissue in complex Freund's adjuvant and hyperacute experimental allergic encephalomyelitis in rats similarly sensitized but with the addition of B. pertussis. Perivascular cuffing, though present, was less pronounced than in other species. There was a prominent polymorphonuclear response, and extravasation of fibrin and red cells occurred. Primary demyelination was a transient, early feature of the disease process in mice, but nerve fiber depletion and gliosis occurred as the disease progressed. The observed myelin degradation most commonly involved the ingestion by macrophages of small fragments of dissociated myelin via crypts or infoldings of the cell surface, at the bases of which were pinocytic, coated vesicles. A similar pattern of myelin breakdown has been described in mouse hepatitis virus encephalomyelitis and multiple sclerosis.
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PMID:Neuropathology of experimental allergic encephalomyelitis in inbred strains of mice. 740 30

Immunization of female SJL mice with an emulsion of lyophilized mouse spinal cord, pertussis vaccine, and complete Freund's adjuvant produces a delayed and often relapsing form of experimental allergic encephalomyelitis (DR-EAE). The mice develop initial signs of disease an average of 6 mo after immunization. Relapses occurred 2 wk to 11 mo after the initial illness. Some animals had multiple relapses. Pathologic examination of the brain and spinal cord revealed perivascular infiltration of mononuclear cells with acute demyelination. Areas of subacute and chronic demyelination ("plaques") were also seen. This model produces a clinical course of relapsing-remitting disease with pathologic evidence of both recent and old inflammatory lesions at various levels of the central nervous system. It thus more closely resembles multiple sclerosis than acute EAE.
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PMID:Delayed, relapsing experimental allergic encephalomyelitis in mice. 746 32

Pregnant rats challenged with Bordetela Pertussis vaccine, with or without encephalitogenic antigen during pregnancy, transferred a resistance to induction of experimental autoimmune encephalomyelitis (EAE) to their offspring. Cross-fostering experiments showed that the protection against EAE is conferred during the lactation period through the transfer of anti pertussis antibodies in the milk. The degree of protection correlated with antibody levels. Passive transfer of these antibodies through intraperitoneal injection to naive adult rats also conferred the same degree of protection against EAE induction. It is suggested that such transfer of resistance and antibodies may serve as a model for the study of milk transmitted immunocompetent factors, as well as a model for the mechanisms involved in the resistance to EAE.
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PMID:Natural and experimental transfer of anti-Pertussis antibodies confers resistance to experimental autoimmune encephalomyelitis. 767 36

We constructed a transgenic mouse model that mimics the human autoimmune disease multiple sclerosis in its spontaneous induction and pathology. Transgenic mice were constructed expressing genes encoding a rearranged T cell receptor specific for myelin basic protein (MBP). T cell tolerance was not induced in the periphery, and functional, autoreactive T cells were found in the spleen and lymph nodes of these mice. Transgenic mice developed experimental allergic encephalomyelitis (EAE) following immunization with MBP and adjuvant plus pertussis toxin as well as with administration of pertussis toxin alone. Spontaneous EAE can develop in transgenic mice housed in a non-sterile facility but not in those maintained in a sterile, specific pathogen-free facility. This model system affords a unique opportunity to dissect the genetic and environmental variables that may contribute to the development of spontaneous autoimmune disease.
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PMID:Transgenic mice that express a myelin basic protein-specific T cell receptor develop spontaneous autoimmunity. 767 52


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