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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent work has implicated plasminogen activator released from macrophages as a possible mediator of the demyelinating process in experimental allergic encephalomyelitis and multiple sclerosis (MS). We have studied the capacity of white matter and plaques from MS patients to break down fibrin clots, using a histochemical technique. Fibrinolytic activity was localized exclusively to areas around blood vessels and capillaries in both patients and controls. While there was marked variation between individuals, the unaffected white matter from MS patients was, on the average, not more active than that of controls, but plaques tended to show more numerous foci of lysis, often also more intense, than adjacent white matter; there was no correlation with disease activity or age of the plaques as determined by histological criteria. The localization and degree of fibrinolysis observed were not related to the presence of lymphocytic infiltrates, gliosis, or macrophages. However, the findings do not exclude an involvement of fibrinolytic enzymes (although originating from vascular endothelium rather than macrophages) in the genesis of the MS plaque, which commonly starts around a small vein.
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PMID:Fibrinolytic activity of plaques and white matter in multiple sclerosis. 721 4

Two strains of pigeon herpes encephalomyelitis virus BVC 78, a virulent field strain, and BVC 78 T7, a cell-culture-adapted strain, were assayed in embryonated chicken eggs and in chicken-embryo-fibroblast (CEF) cell culture to investigate their cytopathogenicity, growth kinetics, plaque characters, and virulence. In CEF the BVC 78 induced syncytia 24-48 hr postinoculation (PI), while the BVC 78 T7 induced only cell rounding 72 hr PI. The strains differed in growth patterns in CEF. The BVC 78 and BVC 78 T7 strains had respective logarithmic phases at 24 and 72 hr PI and maximum virus yields at 36 and 120 hr PI. The BVC 78 T7 was more cell-associated than the BVC 78, the ratio of cell-bound to cell-free virus was about 2 for the former and near unity for the latter. In CEF the BVC 78 induced plaques 1-2 mm in diameter by the third day PI, while the BVC 78 T7 produced small plaques 0.3-0.5 mm in diameter by the 5th day PI. The BVC T7 strain was of low killing capacity for chicken embryos, in contrast to the high killing capacity of the BVC 78. Pigeons inoculated subcutaneously with the former strain and challenged 21 days later with the virulent strain proved resistant.
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PMID:Viral encephalomyelitis of pigeons. V. Comparative studies of virulent and cell-culture-adapted virus. 743 64

Using synthetic peptides, we have defined the major linear antibody epitopes of Theiler's murine encephalomyelitis virus (TMEV), i.e., A1A (VP1(12-25)), A1Ba (VP1(146-160)), A1Cb (VP1(262-276)), A2A (VP2(2-16)), A2B (VP2(165-179)), and A3A (VP3(24-37)). A time course study with either pooled or individual sera indicates that susceptible SJL mice intracerebrally infected with TMEV strongly and selectively recognize the A1Cb epitope of VP1, compared with resistant BALB/c or C57BL/6 mice, which broadly recognize most of the epitopes on the different capsid proteins. However, antibodies from SJL mice subcutaneously immunized with TMEV recognize primarily A1Ba, A1Cb, and A2A epitopes. A similar predominant recognition of the A1Cb epitope was found with antibodies from the cerebrospinal fluid of intracerebrally virus-infected SJL mice. Interestingly, a substantial level of antibodies against the A1Cb epitope in virus-infected SJL mice is of the immunoglobulin G2a subclass, in contrast to an undetectable level of this immunoglobulin G subclass in virus-immunized SJL mice. The level of in vitro viral neutralization by antibodies did not correlate with the clinical signs. Antibodies to A1Cb, A2A, and A2B were able to neutralize viral plaque formation in vitro, while antibodies to A3A, A1A, and A1Ba were not.
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PMID:Analysis of antibody responses to predominant linear epitopes of Theiler's murine encephalomyelitis virus. 751 62

Chronic relapsing experimental autoimmune encephalomyelitis, a demyelinating disease induced by injection of central nervous system (CNS) tissue, is widely used as a model for multiple sclerosis. However, it is unclear which Ag or combination of Ags in the CNS induce the demyelinating immune response. We now show in Lewis rats that a single injection of myelin oligodendrocyte glycoprotein, a specific CNS myelin component, or an appropriately derived myelin oligodendrocyte glycoprotein peptide produces a relapsing remitting neurologic disease with extensive plaque-like demyelination. Igs from affected animals reacted specifically with myelin oligodendrocyte glycoprotein and stimulated a myelin protease activity, leading to myelin basic protein degradation. The demonstrated involvement of myelin oligodendrocyte glycoprotein as a new demyelinating neural Ag may provide a deeper insight into the pathogenesis of multiple sclerosis and its treatment.
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PMID:Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis. 753 10

Activation of astrocytes and hypertrophy of their processes is a result of a number of pathological conditions in the central nervous system. Astrocytic gliosis is especially prominent in multiple sclerosis (MS), where astrocytic fibers form a dense matrix around demyelinated axons. Experimental allergic encephalomyelitis (EAE), a laboratory model for MS, is also accompanied by astrocytic hyperactivity. We have previously shown the formation of plaque-like structures which stain heavily for glial fibrillary acidic protein (GFAP) in the brains and spinal cords of SJL/J mice after several episodes of chronic relapsing EAE (Smith and Eng: J Neurosci Res 18:203, 1987). To further investigate the mechanisms of this phenomenon, we have measured the levels of mRNA for GFAP throughout the course of three episodes and recoveries of EAE in the SJL/J mouse. Mice were immunized with spinal cord homogenate and subsequently developed EAE. After recovery they were again immunized at appropriate intervals, resulting in successive episodes of EAE, with partial or complete recovery between the paralytic stages. At appropriate times in the course of the different stages of EAE, spinal cords were dissected and RNA was prepared from each spinal cord. RNA was analyzed by Northern blots to determine the levels of mRNA for GFAP and, as a control for the 70 kDa neurofilament (NF-L). With the onset of the first EAE episode GFAP mRNA in spinal cords from animals with mild symptoms increased to sixfold the control level (P < 0.02) and to 20-fold in those with paralysis (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:GFAP mRNA fluctuates in synchrony with chronic relapsing EAE symptoms in SJL/J mice. 759 Oct 33

Multiple sclerosis (MS) is probably caused by multiple factors, but there is evidence that an autoimmunological process is relevant for the pathogenesis. Cytokines can operate in different ways in MS and the animal model "experimental allergic encephalomyelitis (EAE). "Interferon gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), TNF-beta, interleukin-1 (IL-1) and IL-2 are important inflammation mediators within the MS plaque, whereas IFN-alpha, IFN-beta, transforming-growth-factor-beta (TGF-beta) and IL-10 exert mainly immunosuppressive functions. Application of these anti-inflammatory cytokines and the selective block of pro-inflammatory cytokines are promising new therapeutic strategies with fewer side effects than the commonly used cytostatic drugs.
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PMID:[Pathogenesis and therapy of multiple sclerosis. The role of cytokines]. 771 57

A set of Theiler's murine encephalomyelitis virus mutants with engineered alterations in the conserved oligopyrimidine/AUG tandem (E. V. Pilipenko, A. P. Gmyl, S. V. Maslova, G. A. Belov, A. N. Sinyakov, M. Huang, T. D. K. Brown, and V. I. Agol, J. Mol. Biol. 241:398-414, 1994) were assayed for their growth potential in BHK-21 cells (as reflected in plaque size) and for neurovirulence upon intracerebral inoculation of mice. Tandem-destroying mutations, which included substitutions in the oligopyrimidine moiety and extended insertions into the oligopyrimidine/AUG spacer, exerted relatively little effect on the plaque size but ensured a high level of attenuation. The attenuated mutants exhibited remarkable genetic stability upon growth in BHK-21 cells. However, the brains of rare animals that developed symptoms after the inoculation with high doses of these mutants invariably contained pseudorevertants with the oligopyrimidine/AUG tandem restored by diverse deletions or an AUG-generating point mutation. The AUG moiety of the tandem in the revertant genomes was represented by either a cryptic codon or initiator codon. The results demonstrate that the tandem, while dispensable for the Theiler's murine encephalomyelitis virus growth in BHK-21 cells, is essential for neurovirulence in mice. Thus, the oligopyrimidine/AUG tandem is a host-dependent cis-acting control element that may be essential for virus replication under certain conditions. The functional activity of the tandem was retained when its oligopyrimidine or AUG moieties were made double stranded. A possible role of the tandem in the cap-independent internal initiation of translation on the picornavirus RNA templates is discussed.
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PMID:Attenuation of Theiler's murine encephalomyelitis virus by modifications of the oligopyrimidine/AUG tandem, a host-dependent translational cis element. 781 54

A sensitive and specific colorimetric dot assay following polymerase chain reaction (PCR) method has been developed to detect 0.1 pg of eastern equine encephalomyelitis viral (EEEV) RNA. The assay is 250-fold more sensitive than analysis by electrophoresis and is based on converting a 291-nucleotide sequence of the viral coat protein amino terminus into a double-stranded DNA (dsDNA) and amplifying the DNA using a specific primer pair and PCR. The amplified complementary DNA (cDNA) is denatured adsorbed onto a nylon strip, baked, and detected with a digoxigenin-labeled probe. Dots with viral cDNA are stained dark red, whereas controls do not stain or stain lightly. The assay is very specific and sensitive and detects only EEEV. RNA of Venezuelan equine encephalitis, St. Louis encephalitis, Keystone, Flanders, Tensaw, and western equine encephalitis viruses were not detected. EEEV (Ten Broeck) RNA was detected at the 10-ng level, indicating that the prototype we used may have different nucleotides in the region where the primer pair binds. The PCR amplified EEEV cDNA that was 92% homologous to the consensus sequence of EEEV. The detection of EEEV in the liver of an infected Emu bird and in field-collected mosquitoes from Florida and Massachusetts that were analyzed concurrently as blind samples by tissue culture plaque assay and by PCR dot analysis proved that the assay is sensitive and can be used to detect infected mosquitoes. The assay can detect at least 1 infected mosquito in a pool of 1,000 uninfected mosquitoes.
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PMID:Sensitive and specific colorimetric dot assay to detect eastern equine encephalomyelitis viral RNA in mosquitoes (Diptera: Culicidae) after polymerase chain reaction amplification. 786 41

This study deals with the relationship between the immunosuppression induced by electrolytic lesions placed into the nucleus locus cerules and the immunopotentiation produced by micromagnets implanted to the parietal area of the skull. The following groups of rats were set up: LC, rats with lesioned locus ceruleus; ShL, sham-lesioned animals bearing non-magnetic beads in the brain parietal region; M, rats with micromagnets of 60 mT influx density in the parietal part of the skull; LCM, animals with impaired locus ceruleus and magnetic beads placed in the parietal area of the skull; and IC, intact control rats. Animals of all groups were tested for plaque-forming cell response, circulating antibodies to sheep red blood cells and bovine serum albumin, Arthus and delayed hypersensitivity skin reactions to bovine serum albumin and old tuberculin, and experimental allergic encephalomyelitis. In LC-rats, humoral and cell-mediated immune reactions were compromised. On the other hand, immune responses in M-rats were significantly potentiated. In LCM-rats, however, the immunosuppression induced by destruction of the locus ceruleus was abrogated by prolonged exposure of the brain parietal region to the magnetic fields, i.e. immune reactivity of LCM-rats was quite similar to that of control IC- and ShL-animals. Several mechanisms may account for the immunomodulating effects produced by lesioning of the locus ceruleus and exposure of the brain to magnetic fields. Noradrenergic, serotoninergic, dopaminergic and peptidergic neurotransmitters, as well as growth hormones and immunopeptides, produced within the central nervous system or elsewhere, may be implicated as necessary for the interactions among the brain, immune apparatus and magnetic fields.
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PMID:Locus ceruleus and immunity. III. Compromised immune function (antibody production, hypersensitivity skin reactions and experimental allergic encephalomyelitis) in rats with lesioned locus ceruleus is restored by magnetic fields applied to the brain. 791 7

Two models of demyelinating experimental allergic encephalomyelitis (EAE) were studied on Lewis rats in whom the disease was induced by injections of either (i) lentil-lectin binding myelin glycoproteins plus myelin basic protein (MBP)-specific T cells (36 rats), or (ii) myelin/oligodendrocyte glycoprotein-specific monoclonal antibody plus MBP-specific T cells (16 rats). In our 24 control rats, 20 received MBP-specific T cells only, and four received myelin glycoproteins plus purified protein derivative-specific T cells. The extent of the resulting blood-brain barrier (BBB) permeability, vasogenic oedema and/or demyelination was assessed in vivo using magnetic resonance imaging (MRI) techniques. The results show that in both demyelinating EAE models the disease appeared more quickly, progressed very rapidly and was more severe than when induced with a similar number of MBP-specific T cells alone. Almost all animals developed hyperacute EAE, with a very high mortality rate. MRI showed a very intense BBB breakdown and vasogenic oedema in all the normally 'leaky' areas of the central nervous system, and focal lesions corresponding to plaque formation in the brain stem or spinal cord near the 'leaky' areas. During the 40-day observation period, the rare survivors of this hyperacute form of EAE presented a chronic form of EAE with serious sequelae. Our results demonstrate that the synergistic effect observed between MBP-specific T cells and antibodies to myelin glycoproteins, especially to myelin/oligodendrocyte glycoprotein, does not only induce demyelinating lesions and chronic clinical signs, but is further responsible, via the normally 'leaky areas', for the fatal increase of the BBB breakdown and vasogenic oedema of which there are ample acute clinical signs.
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PMID:Magnetic resonance imaging of antibody-mediated demyelinating experimental allergic encephalomyelitis. 792 2


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