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)

To investigate the sequence of immunopathologic events during lesion formation in acute experimental allergic encephalomyelitis (EAE), SJL/J mice were inoculated with isogeneic spinal cord in complete Freund's adjuvant (CFA) and with Bordetella pertussis on Days 1 and 3 postinoculation (PI). Mice were sampled at different time points PI and T cells, T-cell subsets. Ia+ cells, Ig+ cells, albumin, and Ig deposits were localized in frozen sections by the avidin-biotin complex (ABC) method and direct fluorescence. Furthermore, samples were stained for Ia antigen, myelin basic protein (MBP), and galactocerebroside (GC) localization on endothelial cells by the ABC technique. Clinical and pathologic observations were correlated with the immunopathologic results. It was found that early in the disease process myelin and Ia-antigens were demonstrable on endothelial cells within the central nervous system (CNS). Simultaneously, damage to the blood-brain barrier was apparent, as indicated by albumin deposits, and small numbers of infiltrating T cells, T-cell subsets, and Ia+ cells were found. With time PI, the density of infiltrating total T cells (Thy-1.2+), helper/inducer (Lyt-1+), and suppressor/cytotoxic (Lyt-2+) T cells increased; Lyt-1+ and Lyt-2+ cells were detectable in meningeal as well as parenchymal infiltrates, while later on, Lyt-1+ cells showed some predilection for the CNS parenchyma and Lyt-2+ cells for meninges. Ia+ cells (B cells, macrophages, activated T cells) were present in small numbers only. Ig+ cells (B cells and macrophages) appeared shortly before onset of signs and persisted in moderate numbers. These results reconfirm the importance of early T-cell involvement for the development of EAE; they might also indicate a secondary role for Ig+ cells and are consistent with the concept that presentation of myelin antigens to T cells might occur locally on Ia-bearing endothelial cells within the CNS.
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PMID:Acute experimental allergic encephalomyelitis in the mouse: immunopathology of the developing lesion. 257 95

Mechanisms involved in the loss of blood-brain barrier function in Lewis rats with experimental autoimmune encephalomyelitis (EAE) were examined using horseradish peroxidase (HRP) as a tracer. In animals injected with HRP before fixation, tracer was observed in two intracytoplasmic compartments: multivesicular bodies (presumably secondary lysosomes) and transcytotic vesicles. Quantitative morphometry of electron micrographs of capillary endothelial cells demonstrated a 5.2-fold increase in these vesicles. This increase in vesicular transport was associated with a decrease in mitochondrial content from 13.7% of the endothelial cytoplasmic area in the normal rat to 4.2% in EAE rats at the height of clinical disease. These alterations correlated with the clinical course of EAE. In animals infused with tracer after fixation, tracer was restricted to areas of cellular inflammation. Immunogold staining of endogenous albumin demonstrated the presence of albumin in cytoplasmic vesicles and in channel-like tubular structures adjacent to endothelial cell junctions. These results indicate that there is a role for vesicles in transendothelial cell transport and edema formation in animals with EAE.
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PMID:Increased vesicular transport and decreased mitochondrial content in blood-brain barrier endothelial cells during experimental autoimmune encephalomyelitis. 259 75

To investigate early immunopathologic events, SJL/J mice were challenged for acute experimental autoimmune encephalomyelitis (EAE) and sampled between 12 hr and 14 days postinoculation (PI). Complete Freund's adjuvant (CFA)-inoculated mice served as controls. T cells, T cell subsets, Class II major histocompatibility (MHC) antigen (Ia)-positive and immunoglobulin (Ig)-positive cells, albumin and Ig deposits, and myelin antigens were localized in frozen sections of central nervous system (CNS) and non-CNS tissue (heart, liver, kidney) by immunocytochemical techniques. In both experimental groups, a few Ia-positive endothelial cells and low-grade diffuse infiltration by T cells, T cell subsets, and Ia+ and Ig+ cells were seen from 12 hr PI onward in CNS and non-CNS tissue. Only in acute EAE but not in CFA-challenged mice were these early changes followed at 10 days PI by extensive inflammation which was restricted to the CNS and was accompanied by Ia-positive astrocytes. Thus, in acute EAE, immunopathologic changes appear to develop in two stages. During the early low-grade generalized phase, recirculation of lymphocytes is moderately enhanced while during the late phase, extensive immunopathology is focused upon the target organ, the CNS.
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PMID:Detailed analysis of early immunopathologic events during lesion formation in acute experimental autoimmune encephalomyelitis. 278 75

The early history of experimental allergic encephalomyelitis is reviewed from the point of view of the characterization and recognition of myelin basic protein and the active agent in acid-fast bacilli, namely muramyl dipeptide. Protocols effective in inducing demyelination are pinpointed. Special attention is paid to the protocol which depends on pretreating guinea pigs with muramyl dipeptide and foreign protein followed by a second injection of foreign protein and then the animals are injected with myelin basic protein and Freund's complete adjuvant. Variations in the timing and amounts of muramyl dipeptide are described as are their effects on the demyelination. The myelin breakdown has been studied with a monoclonal antibody reactive to P2. Similar pretreatment enhances the demyelination in Semliki Forest virus infection in mice. The changes in the blood brain barrier are found at 7 days after the myelin basic protein is injected and show grossly increased uptake by the cerebral vascular endothelium of IgG and perivascular uptake of IgG. The changes in the cerebrospinal fluid (CSF) proteins are described (IgG and albumin). Studies of P2 protein in the CSF by means of a new ELISA technique have been performed on human CSF in multiple sclerosis.
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PMID:Immunological and cytological studies of autoimmune demyelination and multiple sclerosis. 307 85

The intrathecal humoral immune response was analysed in patients with subacute sclerosing panencephalitis (SSPE) and Lewis rats with subacute measles virus (MV)-induced encephalomyelitis (SAME). SSPE patients as well as SAME rats revealed oligoclonal, intrathecal antibody synthesis with MV specificity. SAME rats synthesized MV-specific antibodies intracerebrally to a higher extent than SSPE patients. Although a restricted isoelectric pattern of MV-specific antibodies was detected in the cerebrospinal fluid (CSF) of SSPE patients as well as of SAME rats, the heterogeneity within clusters of immunoglobulin bands was higher in the rat specimens. Increase in the blood-brain barrier permeability for albumin was exclusively detected in SAME rats but not in SSPE patients. These data suggest that the rat model offers excellent opportunities to study the initial humoral events in MV-induced encephalitides.
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PMID:Comparative analysis of virus-specific antibodies and immunoglobulins in serum and cerebrospinal fluid of subacute measles virus-induced encephalomyelitis (SAME) in rats and subacute sclerosing panencephalitis (SSPE). 326 24

The age of sensitization determines the clinical course of experimental allergic encephalomyelitis (EAE) in the guinea pig. Adult animals immunized with central nervous system (CNS) tissue develop acute, fulminant EAE, whereas a relapsing-remitting illness resembling multiple sclerosis occurs if sensitization occurs in the first 2 weeks of life. This study characterized the changes in the proton nuclear magnetic resonance (NMR) relaxometry and imaging of the CNS during the immediate postnatal period. T1 and T2 relaxation times in cerebral hemispheres and spinal cords of strain 13 guinea pigs were consistently prolonged at birth, progressively shortened in the first few weeks of life, and achieved adult levels by age 6 to 11 weeks. There were no age-dependent differences in T1 and T2 relaxation times and tissue specific gravity in either strain 13 or Hartley guinea pigs following immunization with complete Freund's adjuvant, an agent previously reported to disrupt the blood-brain barrier to IgG and albumin in strain 13 guinea pigs. The CNS of neonatal guinea pigs appeared well myelinated by light microscopy and there was no apparent difference in the extent of myelination between newborn and adult animals. Although it was possible to distinguish gray from white matter in the cervical spinal cord of newborn guinea pigs by magnetic resonance imaging (MRI) techniques, gray/white contrast was less satisfactory in the cerebral hemispheres until approximately 6 weeks of life when it was possible to differentiate gray matter, white matter, and cerebrospinal fluid. This study indicates that NMR relaxation times change during early postnatal life, at a time corresponding to the unexplained differences in susceptibility to an immune challenge. These developmental changes appear to be independent of the degree of CNS myelination.
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PMID:Postnatal NMR changes in guinea pig central nervous system: potential relevance to experimental allergic encephalomyelitis. 336 77

Experimental allergic encephalomyelitis (EAE) was induced in young male Lewis rats. Immunohistochemical visualisation of albumin and IgG in the nervous tissue was performed at intervals after induction. The results were correlated to the histological appearance of the tissue. Albumin appeared in the tissue about day 10, 1-2 days before IgG. Within one day both proteins spread from sharply defined perivascular subpial locations to diffuse distribution throughout the tissue. Cellular inflammation was not seen until 3-4 days after extravasation of proteins. The cells also spread from perivascular locations to a diffuse infiltration of the tissue.
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PMID:The distribution of immunoglobulins and albumin in the central nervous system in acute experimental allergic encephalomyelitis. 351 28

Prazosin, an antagonist of the alpha 1-adrenoceptor, has been found to suppress the clinical and histologic expression of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. This effect appears to be specific for the alpha 1-receptor. To determine the effect of this drug on vascular permeability to serum proteins and inflammatory cells, leakage of serum proteins into the central nervous system (CNS) was measured with [125I]albumin, and quantitation of cellular inflammation was determined by an estimation of total DNA. The results show that in both actively induced and passively transferred models of the disease, treatment with prazosin significantly suppresses leakage of serum proteins into the CNS but does not significantly suppress the increase of DNA. The results of the [125I]albumin studies additionally support the conclusion that the extent of vascular permeability to serum proteins in the spinal cord is a significant correlate of clinical disease. The results of the DNA estimation were at variance with the histologic evidence of cellular infiltration. We conclude that treatment with prazosin has a significant effect on the development of vascular edema in EAE. These results additionally validate a role for the adrenergic receptor in the development of EAE, and support the hypothesis that the primary site of action of prazosin is on the vascular alpha 1-adrenoceptor.
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PMID:Prazosin treatment suppresses increased vascular permeability in both acute and passively transferred experimental autoimmune encephalomyelitis in the Lewis rat. 378 88

Myelin basic protein (MBP) of guinea pig origin was incorporated into magnetically responsive albumin microspheres. Protein-protein bonding and stabilization of the GPMBP microspheres by heating at 120 degrees C did not adversely influence their capacity to bind anti-MBP antibodies or demonstrably alter the encephalitogenic activity of the incorporated GPMBP. The magnetic properties of the particles and the fact that immunodeterminants of some of the incorporated MBP fortuitously were distributed on the exterior surfaces of the microspheres allowed a number of experiments to be carried out in Lewis rats for the first time: (a) selective capture and deletion of that particular subpopulation of lymphoid cells responsible for transfer of experimental allergic encephalomyelitis (EAE) represented within the lymph node cells (LNC) of donor animals sensitized to neutral antigen, (b) enhancement of in vivo uptake of MBP by macrophages (M phi s) contained in oil-induced peritoneal cell exudates and exposed briefly to MBP microspheres, and (c) preparation of cell suspensions specifically enriched with respect to MBP-containing M phi s.
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PMID:Albumin magnetic microspheres: a novel carrier for myelin basic protein. 618 46

We studied various biological activities of crystalline pertussigen and found that in mice as little as 0.5 ng of pertussigen induced hypersensitivity to histamine, 8 to 40 ng induced leukocytosis, 2 ng increased production of insulin, 0.1 ng increased production of immunoglobulin E and immunoglobulin G1 antibodies to hen egg albumin, 9.5 ng increased susceptibility to anaphylactic shock, and 0.5 ng increased the vascular permeability of striated muscle. We also found that in Lewis rats 20 ng of pertussigen promoted the induction of hyperacute experimental allergic encephalomyelitis. Pertussigen given intraperitoneally was toxic to mice at a dose of 546 ng. Treatment of pertussigen with glutaraldehyde eliminated this toxicity. Mice immunized with 1,700 ng of detoxified pertussigen were protected against intracerebral challenge with 3 x 10(4) viable Bordetella pertussis cells. When as little as 0.5 ng of pertussigen was given intravenously to mice, the increased susceptibility of the animals to histamine could still be detected 84 days later. The biological properties of crystalline pertussigen indicate its similarity to leukocytosis-promoting factor, Islet-activating protein, late-appearing toxic factor, and mouse-protective antigen of B. pertussis.
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PMID:Biological activities of crystalline pertussigen from Bordetella pertussis. 626 99


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