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)

Results are reported of experiments designed to focus at attachment sites of inflammatory cells (ICs) on the luminal surface of brain endothelial cells (ECs) and on the mechanisms of horseradish peroxidase (HRP) transport across the altered blood-brain barrier (BBB) in a murine model of chronic relapsing experimental allergic encephalomyelitis. Cationized ferritin (CF) served as a marker for evaluating the electrostatic nature of brain microblood vessels (MBVs) on the plasma membranes of ICs or normal mouse peripheral white blood cells and erythrocytes. SJL/J mice demonstrating clinical illness were given HRP or CF, in vivo or in situ, respectively. Light microscopy and conventional transmission electron microscopy of cerebellum or thoracic and lumbar spinal cord regions demonstrated HRP leakage most pronounced in MBVs with perivascular infiltrates. HRP traversed across the ECs via numerous vesicles and tubular profiles located mostly in the parajunctional regions, while EC junctions appeared closed. Scanning electron microscopy demonstrated that IC attachment was primarily at parajunctional sites on the EC surface. We also observed increased microvillar projections extending from the EC surface into the lumen. CF demonstrated a patchy decoration on both the luminal EC surface and IC membranes but did not label uncoated invaginating membrane pits or tubular structures. Our data indicate that the points of attachment of the ICs on the EC surface may reflect specific receptor sites where the ICs eventually gain entrance into CNS across the BBB during brain inflammation.
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PMID:Sites of egress of inflammatory cells and horseradish peroxidase transport across the blood-brain barrier in a murine model of chronic relapsing experimental allergic encephalomyelitis. 278 47

We studied the effect of antioxidant enzymes on the loss of integrity of the blood-brain barrier in the optic nerves of strain-13 guinea pigs with chronic experimental allergic encephalomyelitis, a demyelinating disorder with neurologic and histopathologic characteristics similar to multiple sclerosis. Animals with experimental allergic encephalomyelitis received daily intraperitoneal injections of either preservative-free saline (group 1), catalase (group 2), or glutathione peroxidase (group 3) for 2.2 months after the onset of appendicular paralysis. Following intravascular administration, extravascular leakage of horseradish peroxidase was histopathologically graded as mild, moderate, or severe within the optic nerve head and myelinated retrolaminar nerve. Severe extravasation of horseradish peroxidase was exclusive to group 1, in addition to moderate and mild leakage. In groups 2 and 3, leakage of horseradish peroxidase was infrequent, and when detected, it was graded as mild. Detoxification of hydrogen peroxide with catalase and glutathione peroxidase substantially reduced horseradish peroxidase leakage in experimental optic neuritis, suggesting a role for hydrogen peroxide and its reactive by-products in the pathogenesis of increased vascular permeability of the blood-brain barrier in experimental allergic encephalomyelitis.
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PMID:Antioxidant enzymes reduce loss of blood-brain barrier integrity in experimental optic neuritis. 278 67

The Theiler's murine encephalomyelitis viruses (TMEV) are important neurotropic picornaviruses because they persist in the central nervous system (CNS) and produce an inflammatory demyelinating disease in the mouse, their natural host. Insight into the pathogenesis of this disease may come from studying the genetic and biochemical compositions of these viruses; therefore, in this report, the structural and nonstructural proteins specified by both highly and less virulent TMEV were examined. Using two-dimensional gel electrophoresis, structural and nonstructural proteins, originating from each of the three regions of the picornavirus genome (Kitamura et al., 1981; Rueckert and Wimmer, 1984), from nine TMEV isolates were compared on the basis of isoelectric points (pI). Proteins of two virulent TMEV (GDVII and FA viruses) had almost indistinguishable pI values, whereas two of the three major capsid proteins of the less virulent TMEV varied considerably. For example, the structural proteins VP1 and VP3 from seven less virulent viruses ranged from pI 6.3 to 6.9 and 6.5 to 8.3, respectively. On the other hand, the pI values of VP2 and nonstructural proteins from the less virulent TMEV varied relatively little. In general, structural proteins of each TMEV group had pI ranges unique to their respective biological group, while most nonstructural proteins were similar for all TMEV. The virus-specified proteins of Vilyuisk virus, which is serologically related to the TMEV and a possible cause of encephalomyelitis in man, had pI values similar to the less virulent TMEV. Finally, VP3 not only showed the greatest variation in pI among the less virulent TMEV, but it also was preferentially radioiodinated in intact virus from each of the two biological groups using the lactoperoxidase technique.
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PMID:Comparison of structural and nonstructural proteins of virulent and less virulent Theiler's virus isolates using two-dimensional gel electrophoresis. 298 56

Intracerebral inoculation of murine coronavirus JHM into 2- to 3-day-old Wistar Furth rats causes an acute encephalomyelitis, while inoculations at 10 days of age usually result in hind leg paralysis. To examine the distribution of viral antigens within this infected central nervous system (CNS) tissue, we used the avidin-biotin-peroxidase method to detect monoclonal and polyclonal antibodies bound to JHM structural proteins; in addition we used the Western blot technique to detect viral proteins. Our study demonstrated the following characteristics: Infected neuronal and glial cells produced viral nucleocapsid and E2 glycoprotein. The synthesis of these viral structural proteins was not restricted to cells in any particular part of the central nervous system. While JHM E2 proteins could be detected in individual cells of JHM-infected CNS tissue, the relative level of detectable E2 protein in the total CNS tissue of infected rats was reduced by more than 13-fold compared with JHM-infected tissue culture cells. Hippocampus neuronal cells provided a sensitive indication of JHM infection. These cells invariably contained antigens in both acutely and chronically infected animals. The distribution of cells containing viral antigens differed markedly for JHM-induced acute encephalitis and chronic demyelinating disease. Acutely infected brains had large lesions containing low levels of viral antigen scattered throughout the brain. One percent to ten percent of histologically normal cells in many parts of the brain contained viral antigens; in addition, more neuronal cells than glial cells were observed to be antigen-positive. The hippocampus appeared normal with hematoxylin-eosin staining; however, a scattered infection of neuronal cells was apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of JHM central nervous system infections in rats. 301 91

Using peroxidase immunohistochemistry and in situ hybridization to localize viral antigen and RNA, we studied autopsy tissues from 20 cases of acute fatal human measles (including seven patients with acute encephalomyelitis) and peripheral blood mononuclear cells from 16 patients with acute, nonfatal measles. In immunologically normal patients, virus was detected in five of nine who died five days or less after the onset of rash but in none of 11 who died later. Virus was localized to epithelial cells of lung, gut, bile duct, bladder, and skin and to lymphoid organs. Neither viral antigen nor RNA was detected in brain sections from 14 patients, including seven with acute encephalomyelitis and four with virus identified in other tissues, a finding supporting an indirect pathogenesis of post-measles encephalomyelitis. These data show that measles virus replicates in cells previously not recognized to be involved (capillary endothelium of lymph node and thymus, Hassall's corpuscles, and hepatic duct epithelium) and that invasion of the brain parenchyma during acute measles is uncommon.
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PMID:Acute measles in patients with and without neurological involvement: distribution of measles virus antigen and RNA. 304 79

The authors describe various applications of an immunoblot technique which allows the qualitative determination of the specific antibody activity of oligoclonal IgG intrathecally synthesized in infectious diseases of the nervous system. After dilution of sera to the same IgG concentration as the paired CSF samples, 10 microliters of both fluids are applied side by side on agarose gel plates and isoelectrically focused. Precipitated IgG or specific IgG antibodies are then blotted onto a nitrocellulose sheet previously coated with either a rabbit anti-IgG antiserum or the antigen under study, respectively. The immunoblot is successively incubated with biotinylated anti-IgG antiserum and with the streptavidin-biotin-peroxidase complex before staining with 4 chloro-1-naphthol. This method was applied to samples from patients with subacute sclerosing panencephalitis, herpetic encephalitis, meningoradiculitis due to Herpes Zoster, neuro-AIDS, neurobrucellosis, meningoradiculitis or encephalomyelitis due to Borrelia burgdorferi, and tuberculous meningitis. In each case, specific oligoclonal IgG antibodies, superimposed or not on a diffuse polyclonal synthesis were detected in the CSF, but not, or more faintly, in the corresponding serum. This was taken as evidence for an intra-thecal synthesis of these antibodies. In contrast, when a "mirror effect" was observed, i.e. similar oligoclonal bands in both serum and CSF after dilution at the same IgG concentration, an intra-thecal synthesis was ruled out.
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PMID:[Antibody activity of CSF oligoclonal IgG in infectious neurological diseases. Detection using immunoblotting]. 320 96

A 37-year-old homosexual man with the acquired immune deficiency syndrome (AIDS) developed progressive, ultimately fatal, neurological deficits 12 weeks after a course of cutaneous zoster. Premortem radiological procedures and cerebrospinal fluid analyses were nondiagnostic. At postmortem examination, several opportunistic infections associated with AIDS were recognized. Throughout the brain, necrotic and demyelinative lesions were present, suggestive of progressive multifocal leukoencephalopathy. However, light microscopical examination showed numerous Cowdry type A intranuclear inclusions in astrocytes, oligodendrocytes, and neurons near the periphery of the lesions. Herpes zoster encephalomyelitis was diagnosed and confirmed by electron microscopy, peroxidase-antiperoxidase staining, and by Southern blot analysis of DNA extracted from brain tissue. This case provides insight into the pathogenesis of zoster-associated encephalomyelitis and suggests another agent to be considered in the differential diagnosis of encephalopathy in patients with AIDS and other disorders of immunological impairment.
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PMID:Progressive encephalitis three months after resolution of cutaneous zoster in a patient with AIDS. 396 60

Conjugates of horseradish peroxidase with myelin basic protein (BP) of guinea pig or Lewis rat were used to identify antibody-containing cells in draining lymph nodes during experimental allergic encephalomyelitis (EAE). Peroxidase activity was revealed for light and electron microscopic preparations with the diaminobenzidine reaction of Graham and Karnovsky. Basic proteins (BP) were also iodinated with (125)I for determination of circulating antibody against BP by radio-immunoassay of (125)I BP using coprecipitation with antirat IgG or with antirat serum proteins. Encephalitogenicity was lost after conjugation of guinea pig BP or Lewis rat BP with peroxidase, whereas iodination did not affect the encephalitogenicity of guinea pig or Lewis rat BPs. EAE was induced in Lewis rats with guinea pig or Lewis rat spinal cord BPs in complete Freund's adjuvant. Draining lymph nodes were studied by light and electron microscopy during the course of the immune reaction, and cells with specific antibody against BP were identified with the use of BP-horseradish peroxidase conjugates. Lymph node sections from animals immunized with high antigen doses (500 mug) showed numerous plasma cells with intracellular antibody against BP in medullary cords 10 days after immunization and 4 days prior to histologic appearance of EAE. Numbers of positive cells correlated with levels of circulating antibody against BP. Immunization with a low antigen dose (5 mug) resulted in EAE, few or no antibody-containing cells, and significantly lower levels of circulating antibody. Brown Norwegian rats, a strain resistant to EAE, immunized with 500 mug of BP had positive cells in draining lymph nodes and high levels of circulating antibody against BP in the absence of histologic evidence of EAE. Lewis rats injected with Lewis rat small BP failed to develop EAE. Nevertheless, these animals showed levels of circulating antibody and antibody-containing cells similar to those of animals which developed EAE after injection of the mixture of Lewis rat large and small BP. It is concluded that although the BP-peroxidase labeling method reveals cells with specific anti-BP antibody, these cells are probably unrelated to EAE. The lack of correlation between EAE induced by low antigen doses and levels of circulating anti-BP antibody (determined with the use of highly encephalitogenic (125)I-BP) suggests that effector cells can be stimulated at low antigen doses, but higher antigen doses are required to induce the production of levels of circulating antibody detectable by the method of immune coprecipitation.
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PMID:The significance of circulating and cell-bound antibodies in experimental allergic encephalomyelitis. 454 31

A conjugate of horseradish peroxidase and the encephalitogenic basic protein from myelin has been used to study the antigen reactivity of tissue in the autoimmune disease, experimental allergic encephalomyelitis. Control conjugates were also prepared of peroxidase and bovine serum albumin and of peroxidase and lysozyme, another basic protein. The basic protein from myelin conjugate was specifically bound by lymph node cells from rabbits immunized against the basic protein. Some of these cells appeared to be plasma cells. The conjugate was also specifically bound by occasional cells in the spinal-cord infiltrates of animals with early signs of allergic encephalomyelitis. These cells resembled large lymphocytes and plasma cells. There was no difference between the binding of basic protein of bovine and rabbit origin. The findings suggest the possibility that a local release of antibody within the target organ may play a role in the pathogenesis of allergic encephalomyelitis.
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PMID:Specific binding of peroxidase-labeled myelin basic protein in allergic encephalomyelitis. 528 45

Rabbits sensitized with whole nervous tissue or myelin basic protein (MBP) plus adjuvant and developing experimental allergic encephalomyelitis (EAE) were studied for the presence of oligoclonal immunoglobulin (Ig) bands in spinal fluid and serum. Samples obtained prior to sensitization and at the time of sacrifice were concentrated and subjected to agar gel electrophoresis. Of 11 rabbits receiving whole nervous tissue and developing severe clinical signs of EAE, 7 showed new oligoclonal Ig bands in spinal fluid and in serum obtained 19 days or more after sensitization. With MBP sensitization, 2 of 6 rabbits exhibited new spinal fluid bands, while all 6 rabbits studied demonstrated serum banding. The bands were identified as IgG by immunochemical studies using peroxidase-labeled antisera and by Staph. protein A absorption. The majority of animals showed no banding in presensitization samples. The finding of oligoclonal IgG in EAE reveals yet another immunologic correlation between EAE and the human demyelinating disease, multiple sclerosis.
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PMID:Cerebrospinal fluid and serum oligoclonal IgG bands in rabbits with experiment allergic encephalomyelitis. 616


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