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)

Adoptive transfer of experimental allergic encephalomyelitis (EAE) with splenic lymphocytes from Lewis rats sensitized to myelin basic protein (BP) was potentiated by incubation of the cells in vitro with concanavalin A (Con A). Spleen cells of donors which had recovered from EAE also transferred the disease readily after activation by this procedure. In contrast, the transfer of activity of lymph node cells was not altered. We conclude that during the course of EAE a population of T cells with immunologic memory for BP is generated and persists in the spleen. Incubation with Con A activates these cells and results in marked enhancement of their ability to transfer the disease.
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PMID:Experimental allergic encephalomyelitis: enhancement of cell-mediated transfer by concanavalin A. 30 72

Intraperitoneal administration of pepstatin (2 mg/day for 5 weeks) to Lewis rats subjected to experimental allergic encephalomyelitis (EAE) (induced by guinea pig spinal cord and pertussis vaccine) suppressed the appearance of clinical signs of disease, and reduced the severity and incidence of CNS lesions normally associated with this disease. Administration of pepstatin for shorter periods to Lewis rats, or BSVS mice, or guinea pigs challenged with myelin basic protein delayed, but did not prevent clinical signs of EAE, but was accompanied in all cases by a less severe histopathology.
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PMID:Treatment of experimental allergic encephalomyelitis with an inhibitor of cathepsin D (pepstatin). 30 3

The aim of the so carried out experiments is to establish whether the created disbalance between T- and B-lymphocyte populations influences the final stages of a cell-mediated reaction in vivo. The chosen model was one of experimental autoimmune encephalomyelitis (EAE). Guinea pigs were given a single challenge (intradermally in the hind foot-pads) of 70 microgram myelin basic protein (MBP)--isolated from bovine spinal cord--in complete Freund's adjuvant (CFA). Another group of animals was treated intraperitoneally with 200 mg/kg cyclophosphamide (CY) 3 days before the MBP-CFA challenge. The control group received only CY. At different times after the administration of MBP, CY or CY-MBP, the popliteal lymph nodes have been examined and the morphological changes together with the number of anti-MBP antibody synthesizing cells (ASC) were recorded. In the guinea-pigs treated with the CY 3 days before the antigen challenge the disease develops earlier and shows a degree of severity with a threefold greater mean score. The number of ASC is increasing up till the 10th day and slightly decreases toward the 20th day when there are clinical and histological signs of EAE. If MBP is administered after a 3-day action of CY, the number of these cells till the 7th day after the antigen challenge is strongly reduced, then surpasses the normal value about the 10th day and comes back to it towards the 20th day. The results so obtained confirm the concept of the T-lymphocyte mediation of EAE and give us grounds for discussing the CY action on the lymphocyte subpopulation.
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PMID:[Influence of cyclophosphamide on the production of experimentale autoimmune encephalomyelitis (author's transl)]. 30 38

In order to assess whether experimental allergic encephalomyelitis (EAE), a putative animal model for multiple sclerosis (MS), is an ongoing chronic disorder, we have studied the permeability of spinal cords of Lewis rats with EAE to 3H-uridine- or 3H-thymidine-labeled lymphoid cells obtained from thymuses of naive donors or from draining lymph nodes of donors injected with guinea pig spinal cord + complete Fruend's adjuvant (CFA), guinea pig myelin basic protein + CFA, or with CFA alone. During the acute clinical phase of EAE there is a high-level infiltration of 3H-thymidine- or 3H-uridine-labeled cells into the spinal cords. After clinical recovery from EAE up to 58 days post-inoculation, there is a low-level infiltration of 3H-thymidine-labeled cells into the spinal cords. A similar infiltration into the spinal cords by 3H-uridine-labeled cells was not detected. Donor cells from animals immunized with CFA alone showed similar levels of infiltration into the spinal cords of animals with EAE as donor cells from animals immunized with the encephalitogenic emulsion. Spinal cords from recipients immunized with CFA alone showed no increased permeability to labeled cells. Heat-killed labeled cells did not migrate into the spinal cords of animals with EAE. We conclude that a) EAE is a chronic disease and in this regard is a valid model for MS; and B) in the chronic phase of EAE, recently divided cells (3H-thymidine-labeled cells) show higher levels of migration into the target tissue than 3H-uridine-labeled cells.
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PMID:Chronic permeability of the central nervous system to mononuclear cells in experimental allergic encephalomyelitis in the Lewis rat. 30 23

Lewis rats with experimental allergic encephalomyelitis (EAE) exhibited cell-mediated immunity to myelin basic protein as determined both with in vivo and in vitro assays. Positive skin test reactions and production of migration inhibitory factor (MIF) were observed before onset and after recovery from EAE. Rats rendered unresponsive to EAE exhibited in vitro cell-mediated immunity to basic protein, although in vivo manifestations were depressed. However, tolerant rats failed to respond to the encephalitogenic determinant; rats with EAE exhibited cell-mediated immunity to this region of the molecule. The results indicate that EAE-unresponsive rats possess lymphocytes capable of responding to basic protein, but that reactivity to the encephalitogenic peptide is suppressed.
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PMID:Cell-mediated immunity to myelin basic protein in Lewis rats made unresponsive to experimental allergic encephalomyelitis. 36 47

A radioisotopic index test was used to detect that time of onset and intensity of cell-mediated immune inflammation of experimental autoimmune encephalomyelitis (EAE) in mice. Mice were tested at various time intervals after an encephalitogenic immunization with mouse spinal cord to homogenate for delayed-type hypersensitivity (DTH) to myelin basic protein (MBP) by intradermal challenge with antigen in the ear pinna. After 25 hr, the intensity of DTH was measured by 125I-radiometry which depends upon the migration of 125I-UdR radiolabeled mononuclear cells into the antigen depot. Cells reactive to MBP were detected by the ear assay as early as 7 days after the initial encephalitogenic sensitization. The degree of cell-mediated immune inflammation in the brain and spinal cord during the evolution of EAE was also measured by a radioisotopic technique; increased 125I-UdR uptake could be detected in the brain 3 to 4 days before the onset of signs of EAE at days 11 to 12, whereas 125I-UdR in the spinal cord was detected only 1 day before, or concomitant with, the onset of signs of EAE. Both, or concomitant with, the onset of signs of EAE. Both the "ear" and "organ" radiometric index tests are useful in measuring the degree of cell-mediated inflammation in EAE, and supplement routine histopathological and observational assessments.
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PMID:Measurement of cell-mediated inflammation in experimental murine autoimmune encephalomyelitis by radioisotopic labeling. 47 99

Epsilon aminocaproic acid, an inhibitor of plasminogen and trypsinogen activators, can decrease the severity of experimental allergic encephalomyelitis (EAE) in rats. The drug was tried because of a number of observations suggesting that neutral proteases, such as plasmin, might be chemical mediators of demyelination. The highest concentrations of plasminogen activator are found in the walls of veins and venules, around which demyelination is common in many demyelinating diseases, including MS. Indeed, the earliest lesion in MS is often demyelination with little cellular infiltration. In vitro studies have shown that neutral proteases secreted by activated macrophages selectively lyse myelin basic protein.
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PMID:The modification of experimental allergic encephalomyelitis with epsilon aminocaproic acid. 56 43

Tissue culture studies of human and experimental demyelinating diseases have demonstrated that sera from patients with multiple sclerosis reversibly demyelinate central nervous system cultures. Similar changes are evoked by sera from animals with experimental allergic encephalomyelitis induced by inoculation with whole central nervous system tissue but not by encephalitogenic myelin basic protein. Sera and buffy coat or lymph node cells from humans with idiopathic polyneuritis and animals with experimental allergic neuritis demyelinate cultures of peripheral nervous system tissue. While these studies have contributed to speculations about pathogenetic mechanisms of demyelinating diseases, including the role of both circulating antibodies and delayed hypersensitivity factors, a number of important questions remain unanswered. Among these are the identity of the antigens that evoke antimyelin antibodies and the precise relationship of serum or cellular antimyelin factors to the pathogenesis or clinical course of the demyelinating diseases. Further studies with this technique may provide more complete information about the role of immunological events in induction of disease.
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PMID:Tissue culture studies of demyelinating disease: a critical review. 61 71

The spinal fluid of sheep with experimental allergic encephalomyelitis contains myelin basic protein (6 to 18 nanograms per milliliter) bound to antibody as well as excess free antibody. This bound myelin basic protein appeared concurrently with the onset of the disease and remained elevated until death. In contrast, in active multiple sclerosis, the spinal fluid contains free myelin basic protein and there are no detectable levels of antibody. The results indicate that the antibodies enter the spinal fluid from the serum by passive diffusion. This mechanism may also explain the presence of viral antibodies in the spinal fluid of multiple sclerosis patients.
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PMID:Spinal fluid differences in experimental allergic encephalomyelitis and multiple sclerosis. 61 57

This paper reports the effects of supplementation of the diet with linoleic acid on the severity of experimental allergic encephalomyelitis (EAE) in guinea pigs. Clinical signs of disease (e.g. paresis, paraplegia, urinary incontinence), weight loss, frequency of perivascular lesions in the central nervous system and ability of isolated lymph node cells to respond to myelin basic protein in vitro were all reduced by linoleic acid supplementation. Linoleic acid was effective when fed at a dose of 0.5 ml/day from 7 to 21 days after sensitization of the animals with basic protein, i.e., before and during the time in which clinical signs normally appeared. The same daily dose fed from 7 days before to 7 days after sensitization, i.e., ceasing about 7 days before the normal time of appearance of clinical signs, produced no significant effect. Feeding linoleic acid to normal guinea pigs significantly altered the fatty acid composition of their serum and lymph nodes, but not of their brain. Of several possible explantations for the protective effect of lineolic acid in EAE, we considered action by this essential fatty acid on the immune system most likely.
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PMID:Reduction by linoleic acid of the severity of experimental allergic encephalomyelitis in the guinea pig. 63 36


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