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)

In 1987, follow-up studies were conducted on 72 patients who had had meningoradiculitis and encephalomyelitis (8 patients) due to Borrelia burgdorferi 5-27 years previously. These patients had not been treated with antibiotics, either during the acute disease or during the interval prior to follow-up studies. The patients had exhibited the typical symptoms of Bannwarth's syndrome during the acute phase. At the follow-up studies, 33 patients showed no, and 23 only mild, clinical residual symptoms including normal CSF findings and low-positive serum IgG borrelia antibody titres (IFT; ELISA). Three patients without sequelae exhibited persistent intrathecal secretion of oligoclonal B. burgdorferi-specific CSF IgG antibodies (Immunoblot; positive borrelia CSF IgG antibody titres). Thirteen patients exhibited mild-to-medium sequelae with persistent intrathecal formation of oligoclonal B. burgdorferi-specific CSF IgG antibodies, up to 21 years after the acute illness. This persistence can be interpreted as an "immunological scar syndrome". Our follow-up studies appear to indicate that neurological manifestations of B. burgdorferi infections are generally (with few exceptions) of a benign nature. Most patients can be classified as having been cured without antibiotic therapy. No late manifestations of chronic progressive CNS borreliosis comparable to that of neurosyphilis have been seen following acute untreated neuroborreliosis.
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PMID:Meningoradiculitis and encephalomyelitis due to Borrelia burgdorferi: a follow-up study of 72 patients over 27 years. 279 99

Myelin basic protein (BP) has the capacity to induce experimental allergic encephalomyelitis (EAE) in animals as well as to prevent and suppress EAE. Immunoreactive BP or BP fragments appear in cerebrospinal fluid (CSF) in persons with multiple sclerosis in acute disease periods and in individuals with acute damage to central nervous system myelin. Humoral and cellular immune responses, especially in the CSF, may occur but are of uncertain effect in the etiology and pathogenesis of MS. Attempts to use BP to suppress MS have disclosed no therapeutic benefit.
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PMID:Myelin basic protein and multiple sclerosis. 619 37

The authors present the results of studying encephalomyelitis caused by the neurotropic (IHM) strain of the murine hepatitis virus in 60 mice of the C3H line infected intracerebrally at the age of 4 weeks. Morphological examinations of the brain carried out on the 5th-13th day (the acute period) and the 14th-30th day (the subacute stage) have shown that it is myelin-producing cells that are affected first in this form of encephalomyelitis, while the periaxonal process observed is a consequence of this affection. Proofs of this conclusion are presented. It is shown that in subacute encephalomyelitis, similar processes develop. Degeneration and infection of oligodendrocytes are not so pronounced in that case, as in the acute disease. However, destruction of even individual oligodendrocytes may lead (due to the peculiarities of their structure and function) to an avalanche-like process of demyelinization. It is supposed that the vesicular degeneration of myelin may arise in the sites of close contact between the myelin membranes and the cells of inflammation infiltrates (release of lysosomal enzymes and toxic products formed in edema). In the latter case the viruses serve as an antigen depot that causes and maintains the inflammatory process.
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PMID:[Demyelinization process in acute and subacute experimental encephalomyelitis]. 629 31

The murine coronavirus strain JHM is highly neurotropic in rats and has a marked tendency to cause demyelinating central nervous system diseases after intracerebral inoculation. The clinical diseases observed range from an acute encephalomyelitis occurring within 2 weeks postinfection to a subacute demyelinating encephalomyelitis developing several weeks or months postinfection. Uncloned wild-type virus induced both acute and subacute diseases, whereas cloned JHM virus grown in tissue culture caused only acute disease without the pronounced lesions of primary demyelination. In contrast, temperature-sensitive mutants selected from that clone were capable of inducing subacute demyelinating encephalomyelitis after prolonged incubation times. Viruses recovered from diseased animals were still temperature sensitive. Inoculation of temperature-sensitive mutants into suckling rats (age, 10 to 15 days) produced high rates of subacute demyelinating diseases running a more chronic course; these diseases often were not fatal. Those rats which did not show clinical signs frequently revealed inflammatory demyelinating lesions. These findings indicate that the rate and type of clinical disease are dependent on the neurovirulence of the virus mutant used for inoculation and the age of the animals at the time of infection.
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PMID:Neurovirulence of murine coronavirus JHM temperature-sensitive mutants in rats. 630 92

In immature Strain 13 guinea pigs sensitized to syngeneic spinal cord, a chronic allergic encephalomyelitis is elicited reminiscent of demyelinating diseases of man and which features relapses or progressive downhill course and extensive areas of demyelination in the central nervous system. However, juvenile recipients of syngeneic lymphocytes from similarly sensitized juveniles show only the acute form of experimental allergic encephalomyelitis. Neuropathologically, the CNS of affected animals displayed mild changes only and minimal demyelination. These observations indicate that the age-dependent differences seen between the acute disease of adults and the chronic disease of juveniles may be due to differences in availability of modulating or reparatory factors, rather than differences in the central nervous system organ or in the immune response itself.
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PMID:Adoptive transfer of experimental allergic encephalomyelitis from immature guinea pig donors. 663 43

Mice infected with the neurotropic JHM strain of mouse hepatitis virus (MHV-JHM) develop a demyelinating encephalomyelitis several weeks after infection. Astrogliosis and infiltration of inflammatory cells are prominent findings in the brains and spinal cords of infected mice. In this report, astrocytes in infected spinal cords were analyzed for expression of three pleiotropic cytokines, TNF-alpha, IL-1 beta, and IL-6; Type 2 nitric oxide synthase (iNOS); and MHC class I and II antigen. The data show that all three cytokines and iNOS are expressed by astrocytes in chronically infected spinal cords. These activated astrocytes are localized to areas of virus infection and demyelination, although most of the astrocytes expressing these proteins are not MHV-infected. MHC class I and II antigen can be detected in these spinal cords as well, but not in cells with the typical morphology of astrocytes. TNF-alpha, IL-6, and iNOS are also evident in the brains of mice with MHV-induced acute encephalitis, but in marked contrast to the results obtained with the chronically infected mice, most of the cells expressing these cytokines or iNOS had the morphology of macrophages or other mononuclear cells and very few appeared to be astrocytes. Additionally, astrocytes and, most likely, oligodendrocytes are infected in the spinal cords of mice with chronic demyelination. These results are consistent with a role for both viral infection of glial cells and high localized levels of proinflammatory cytokines and nitric oxide in the demyelinating process in mice infected with MHV-JHM. They also show that analogously to the human demyelinating disease, multiple sclerosis, astrocytes are a major cellular source for these cytokines in mice with chronic, but not acute disease.
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PMID:Activation of astrocytes in the spinal cord of mice chronically infected with a neurotropic coronavirus. 749 73

The role of epitope spreading in the pathology of relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) was examined. Using peripherally induced immunologic tolerance as a probe to analyze the neuropathologic T cell repertoire, we show that the majority of the immunopathologic reactivity during the acute phase of R-EAE in SJL/J mice induced by active immunization with the intact proteolipid (PLP) molecule is directed at the PLP139-151 epitope and that responses to secondary encephalitogenic PLP epitopes may contribute to the later relapsing phases of disease. Intermolecular epitope spreading was demonstrated by showing the development of T cell responses to PLP139-151 after acute disease in mice in which R-EAE was initiated by the transfer of T cells specific for the non-cross-reactive MBP84-104 determinant. Intramolecular epitope spreading was demonstrated by showing that endogenous host T cells specific for a secondary encephalitogenic PLP epitope (PLP178-191) are demonstrable by both splenic T cell proliferative and in vivo delayed-type hypersensitivity responses in mice in which acute central nervous system damage was initiated by T cells reactive with the immunodominant, non-cross-reactive PLP139-151 sequence. The PLP178-191-specific responses are activated as a result of and correlate with the degree of acute tissue damage, since they do not develop in mice tolerized to the initiating epitope before expression of acute disease. Most importantly, we show that the PLP178-191-specific responses are capable of mediating R-EAE upon adoptive secondary transfer to naive recipient mice. Furthermore, induction of tolerance to intact PLP (which inhibits responses to both the initiating PLP139-151 epitope and to the PLP178-191 epitope) after the acute disease episode is sufficient to prevent relapsing disease. These results strongly support a contributory role of T cell responses to epitopes released as a result of acute tissue damage to the immunopathogenesis of relapsing clinical episodes and have important implications for the design of antigen-specific immunotherapies for the treatment of chronic autoimmune disorders in humans.
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PMID:Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis. 754 Jun 58

Immunization of a limited number of rodent strains with central nervous system-derived Ags induces experimental allergic encephalomyelitis (EAE). In contrast to susceptible female SJL mice, age-matched males are resistant to actively induced EAE. The ability of immunization with neuroAg to induce Ag-specific T cell activation in resistant male mice was examined. Ag-specific T cell proliferation was found following immunization of both male and female SJL mice. Draining lymph node cytokine mRNA patterns demonstrated that immunization of EAE-resistant male mice resulted in a Th2-type pattern. By contrast, immunization of EAE-susceptible female mice resulted in a Th1-type pattern. Priming of Th1- and Th2-type responses was confirmed by analysis of cytokines secreted following Ag-specific proliferation. In contrast to the transfer of myelin basic protein (MBP)-specific Th1-type T cells derived from female mice, which induced acute and relapse EAE, transfer of MBP-specific Th2-type T cells derived from male mice resulted in no clinical or histologic evidence of EAE. A mixture of MBP-specific Th1 and Th2 type cells was transferred to naive recipients to determine if the neuroAg-specific Th2-type cells exerted a regulatory influence on EAE. Acute disease was partially eliminated and relapses were completely eliminated in these recipients. Analysis of spinal cords showed the presence of both Th1 and Th2 cytokine mRNAs. These data are consistent with both the ability of Th2-type cells to suppress autoimmunity and a homeostatic mechanism of T cell regulation based on the cross-regulation of Th1 and Th2 cells in the maintenance of peripheral tolerance.
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PMID:Self-antigen-induced Th2 responses in experimental allergic encephalomyelitis (EAE)-resistant mice. Th2-mediated suppression of autoimmune disease. 756 Nov 16

Theiler's murine encephalomyelitis virus (TMEV) is a single-stranded RNA virus that belongs to the family of picornaviruses. Intracranial inoculation of susceptible mouse strains with TMEV results in biphasic disease, consisting of early acute disease that resembles poliomyelitis, followed by late chronic demyelinating disease that is characterized by the appearance of chronic inflammatory demyelinating lesions. Susceptibility to TMEV infection is genetically controlled by three loci: one that maps to the H-2D region of the major histocompatibility complex, one to the beta-chain constant region of the T-cell antigen receptor, and one located on chromosome 3. Both early acute and chronic late demyelinating diseases are immunologically mediated. T cells appear to play an important role in the pathogenesis of the disease. TMEV-induced demyelinating disease in mice has extensive similarities with multiple sclerosis, and it is considered one of the best experimental animal models for multiple sclerosis.
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PMID:Immunology of Theiler's murine encephalomyelitis virus infection. 756 39

Experimental allergic encephalomyelitis (EAE) is considered the animal disease model for multiple sclerosis (MS) in humans. However, EAE is an acute disease whereas MS is a chronic disease. The on-off nature in both diseases of autoimmune reactivity suggests a regulatory response by the host, a response which can effect the autoreactive T cell by modulating-up or modulating-down. This review discusses various aspects of this regulation, seen after administration of autoantigen, of antibody directed at the T cell receptor (TcR), and of fragments of the TcR itself.
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PMID:The ups and downs of EAE. 768 9


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