Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental allergic encephalomyelitis has been induced in guinea pigs using the encephalitogenic tryptophan peptide as antigen and a hydrosoluble adjuvant extracted from Mycobacterium tuberculosis, var. hominis, strain H37Ra. The maximum response was observed using 100mug of adjuvant per animal. This is a quantity of adjuvant substantially higher than was necessary to induce disease utilizing the whole myelin basic protein as antigen.
 ...
PMID:Induction of allergic encephalomyelitis using hydrosoluble adjuvant and the tryptophan region of myelin basic protein. 5 9

Rats of the Lewis strain were fed diets adequate or deficient in essential fatty acids (EFA). At 70-80 days of age experimental allergic encephalomyelitis (EAE) was induced using adjuvants containing either Mycobacterium butyricum or Mycobacterium tuberculois H37Ra. When the former Mycobacterium was used, the incidence of EAE was greater in the EFA-deficient than in EFA-adequate controls; but when the rats challenged with M. tuberculosis, the incidence of the disease was the same in both dietary groups. Brain slices from EFA-deficient rats had a marginally depressed synthesis of prostaglandin F (PGF) compared to that of controls. Immunochallenge with adjuvant alone or adjuvant plus antigen tended to depress further PGF synthesis by brain slices from EFA-deficient rats and significantly depressed synthesis by slices from rats receiving adequate EFA. Whether or not rats were paralyzed had no effect on PGF synthesis when the diet was adequate in EFA, but a significant difference was seen in the EFA-deficient group. The results indicate a possible role for PGF synthesis in the degree of susceptibility of the rats to EAE under different dietary regimens.
 ...
PMID:Cerebral prostaglandin synthesis during the dietary and pathological stresses of essential fatty acid deficiency and experimental allergic encephalomyelitis. 9 86

The changes in the glial cell reactivity depended on the phase and severity of the pathological process in the experimental allergic encephalomyelitis induced in guinea pigs by injection of Mycobacteria tuberculosis in a mixture of arlacel and vaselin. These reactivity changes measured by the method of inhibition of the glial cell migration in the tissue culture was specific of the nervous tissue antigens. The same changes in the reactivity could be induced in the tissue culture of the glial cells from the intact animals by the addition of sera or the lymph node cells from the actively sensitized guinea pigs. The present data did not allow to attribute the changes in the glial cell reactivity to the products of destruction of the nervous tissue only to the action of the humoral or the cell factors (elements) penetrating into the CNS from the blood vessels or the lymphatic tissue.
 ...
PMID:[Reactivity of the neuroglia in guinea pigs sensitized with Mycobacteria tuberculosis]. 81 99

Experimental autoimmune encephalomyelitis (EAE) was induced in inbred and congenic strains of mice by injection of mouse spinal cord homogenate (MSCH) in Freund's complete adjuvant (FCA) with pertussis vaccine. Genetic analyses showed that susceptibility to EAE in mice was inherited as a dominant trait and was in part controlled by genes located in the centromeric half of the H-2 complex. Mice with EAE developed cell-mediated immune responsiveness to basic protein of myelin (BPM), as judged by the macrophage migration inhibition assay, using peritonealyexudate cells; this was not observed with mice of resistant strains. However, the migration of peritoneal exudate cells of both susceptible and resistant strains was significantly inhibited in the presence of purified protein derivative (PPD) of M. tuberculosis. Thus, the genes involved in the control of susceptibility to EAE also influence T cell responsiveness to BPM. Antibody to BPM, as judged by radioimmunoassay, was detected in susceptible and resistant strains but there was no correlation between the presence or levels of antibody and susceptibility or resistance to EAE. It is suggested that resistance to EAE is associated with failure of T cells to recognize and/or respond to the encephalitogenic determinant of the BPM molecule.
 ...
PMID:Experimental autoimmune encephalomyelitis in mice: genetic control of susceptibility. 110 34

To characterize the cellular immune response in an autoimmune lesion, we investigated the accumulation of specific T cells in the central nervous system in actively induced experimental autoimmune encephalomyelitis (EAE) in Lewis rats, using a limiting dilution analysis (LDA) assay for T cells that proliferate in response to antigens. Lymphocytes isolated from the spinal cord infiltrate were compared with cells from the popliteal lymph nodes with respect to frequency of cells responding to basic protein (BP), mycobacterium tuberculosis (MT), the 65-kD heat shock protein (hsp65), allogeneic brown norway spleen cells, and concanavalin A. Additionally, we compared the BP frequency in acute EAE of cells from the spinal cord, peripheral blood, spleen and lymph nodes, and the spinal cord and lymph node after recovery from EAE. We found that acute EAE was associated with marked enrichment of BP-reactive T cells in the spinal cord relative to their frequency in the lymphoid organs and peripheral blood. The infiltrate was also enriched for T cells responding to hsp65; alloreactive T cells, in contrast, were not enriched. The frequency of BP reactive T cells in the spinal cord was highest at the peak of paralysis; however, BP-reactive T cells could still be detected at moderate frequencies after clinical recovery. We established BP- and Mycobacteria-reactive T cell lines from the spinal infiltrates that were CD4+ and TcR alpha beta +. Most of the BP lines were found to react to the major encephalitogenic epitope of guinea pig BP for rats (amino acids 71-90); these lines were found to mediate EAE in naive recipients. T cell lines recognizing other epitopes of BP were not encephalitogenic. All of the lines responsive to Mycobacteria recognized hsp65 or hsp70. These results indicating that the immune infiltrate in active EAE is enriched with cells responding to the autoantigen and to hsp65 were confirmed in EAE adoptively transferred by anti-BP T cell clone.
 ...
PMID:T cells in the lesion of experimental autoimmune encephalomyelitis. Enrichment for reactivities to myelin basic protein and to heat shock proteins. 128 35

Infectious agents have often been implicated in the etiology of autoimmune diseases. Here we show that bacteria may also play a role in resistance to autoimmune diseases. SJL/J and (SJL/J x BALB/c)F1 mice are genetically susceptible to induction of experimental autoimmune encephalomyelitis (EAE), a murine model for human demyelinating autoimmune diseases such as multiple sclerosis. We studied the effect of several bacteria on the development of EAE and found that exposure of SJL/J or (SJL/J x BALB/c)F1 mice to Mycobacterium tuberculosis or Bordetella pertussis consistently rendered mice highly refractory to subsequent induction of the disease. Other bacteria such as Escherichia coli, Shigella and Staphylococcus aureus were found to be less effective, or were protective only if specific immunization procedures were used. Furthermore, M. tuberculosis and B. pertussis were protective irrespective of the route of administration and minute amounts (as low as 0.5 micrograms) of M. tuberculosis were sufficient to protect EAE-susceptible mice against induction of the disease. Interestingly, these bacteria, which are commonly used to promote development of EAE, conferred the highest degree of protection against the disease. The M. tuberculosis-induced protection was found to be associated with active suppression mechanisms mediated by T lymphocytes capable of transferring protection to naive syngeneic mice. These findings indicate that certain bacteria may protect against the development of autoimmune diseases. These results also suggest the potential use for still-unidentified bacterial agents in the manipulation of certain autoimmune diseases.
 ...
PMID:Bacterial agents protect against autoimmune disease. I. Mice pre-exposed to Bordetella pertussis or Mycobacterium tuberculosis are highly refractory to induction of experimental autoimmune encephalomyelitis. 148 83

Susceptibility to experimental autoimmune encephalomyelitis (EAE), which is an autoimmune disease inducible by immunization with a brain-specific antigen in complete Freund's adjuvant (CFA), is different among strains. In an attempt to resolve the immune mechanisms by which the difference in susceptibility to EAE is regulated, we re-estimated susceptibility of several strains of rats, and the frequency of antigen-reactive T cells in each strain was determined by limiting-dilution analysis. EAE was induced in Lewis (LEW), PVG/c and BN rats using four different methods: (i) active immunization with guinea-pig myelin basic protein (GPBP) in CFA; (ii) immunization with GPBP in CFA that had been further supplemented with Mycobacterium tuberculosis H37Ra (supplemented CFA); (iii) adoptive transfer of GPBP-activated spleen cells into syngeneic rats; and (iv) transfer of a GPBP-specific T-cell line. The LEW strain was susceptible to all four methods. The PVG/c strain was resistant to immunization with GPBP in conventional CFA (GPBP/conv. CFA), but was susceptible to immunization with GPBP in supplemented CFA (GPBP/suppl. CFA) and to transfer of activated spleen cells. The BN strain was resistant to all methods. Limiting-dilution analysis using T cells from LEW, PVG/c or BN rats has revealed that each strain of rat displays a different pattern of frequencies of GPBP-reactive or the 68-88 sequence (GP68-88)-reactive T cells. LEW rats showed relatively high frequencies of GPBP-reactive and GP68-88-reactive T cells after immunization with either GPBP/conv. CFA or GPBP/suppl. CFA, symptomatic rats showing higher values than asymptomatic rats. In asymptomatic PVG/c rats, the frequency of GP68-88-reactive T cells was lower than that of GPBP-reactive T cells. In PVG/c rats with clinical EAE, however, GP68-88-reactive T cells increased in frequency and were almost the same as GPBP-reactive T cells. BN rats, on the other hand, responded very poorly not only to the GP68-88 sequence but also to the whole GPBP molecule, even after immunization with GPBP/suppl. CFA. These findings, obtained by limiting-dilution analysis, strongly suggest that the development of EAE in LEW, PVG/c and BN rats is closely related to the frequency of GPBP-reactive T cells. Furthermore, it is shown that resistance to EAE found in PVG/c and BN rats may be generated by different immune mechanisms.
 ...
PMID:Limiting-dilution analysis of the frequency of myelin basic protein-reactive T cells in Lewis, PVG/c and BN rats. Implication for susceptibility to autoimmune encephalomyelitis. 168 93

Oral administration of proteins is a long-recognized method of inducing antigen-specific peripheral immune tolerance. We previously showed that oral administration of myelin basic protein suppresses monophasic experimental autoimmune encephalomyelitis in the Lewis rat when it is given in association with immunization and prior to disease onset. As a potential therapy for human autoimmune disease, it is crucial to determine whether oral tolerance can ameliorate an ongoing immune response. We therefore asked whether oral administration of myelin antigens, after sensitization and disease expression has occurred, could affect immunological, clinical, or pathological features of experimental autoimmune encephalomyelitis. Chronic relapsing experimental autoimmune encephalomyelitis was induced in the Lewis rat and strain 13 guinea pig by immunization with whole guinea pig cord homogenate, complete Freund's adjuvant, and Mycobacterium tuberculosis. Following recovery from the first attack, animals were orally given bovine myelin, guinea pig myelin, or guinea pig myelin basic protein three times per week for up to 3 months. Animals receiving myelin products orally had decreased severity and frequency of clinical relapses, decreased delayed-type hypersensitivity responses to myelin antigens, diminished inflammation in the central nervous system (CNS), and decreased areas of CNS demyelination. In the rat, guinea pig myelin basic protein was as effective as guinea pig myelin in ameliorating the disease and also resulted in decreased serum anti-myelin basic protein antibody levels. No exacerbation of disease or worsening of pathological findings occurred in the animals given myelin products. These results demonstrate that oral administration of myelin antigens can suppress chronic relapsing experimental autoimmune encephalomyelitis and have direct relevance to therapy of human demyelinating disorders such as multiple sclerosis.
 ...
PMID:Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin antigens: IV. Suppression of chronic relapsing disease in the Lewis rat and strain 13 guinea pig. 171 32

The effects of decomplementation by cobra venom factor (CVF) on the pathogenesis of inflammation and demyelination in experimental allergic encephalomyelitis (EAE) and acute antibody-mediated demyelinating EAE (ADEAE) have been quantified histologically and immunocytochemically. In rats immunized with 50 micrograms of myelin basic protein in Freund's complete adjuvant containing 100 micrograms heat-killed Mycobacterium tuberculosis H37Ra, clinical signs of EAE were completely suppressed by two injections of CVF given 9 and 12 days post-immunization. Suppression of clinical disease was associated with a dramatic reduction in peri-vascular inflammation in the CNS, although immunohistochemical staining identified small numbers of infiltrating T cells and macrophages. In contrast, CVF treatment had no significant effect on the clinical severity of ADEAE and although C9 deposition within the CNS was virtually abolished, there was no statistically significant decrease in the extent of demyelination or inflammation. These observations indicate that in the absence of complement components C3 and C5 an antibody-dependent cell-mediated cytotoxic response plays an important role in the pathogenesis of antibody-mediated demyelination. The major role of the complement cascade in EAE appears to be the generation of pro-inflammatory factors that enhance the inflammatory response within the CNS in animals facing a mild encephalitogenic challenge.
 ...
PMID:Antibody-mediated demyelination in experimental allergic encephalomyelitis is independent of complement membrane attack complex formation. 199 58

There is evidence suggesting the involvement of the platelet-activating factor (PAF) in central nervous system (CNS) functions. The possibility exists that PAF may be relevant in eliciting cell-mediated autoimmune phenomena in CNS. To assess the role of PAF in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), male Lewis rats were primed with whole spinal cord from guinea pig, emulsified in Freund's adjuvant supplemented with 10 mg/ml of Mycobacterium tuberculosis, H37Ra strain. Treatment with two different PAF antagonists (PCA 4248, WEB 2170) was applied starting from day 1 or day 5 postinoculation on a twice-daily basis. Neither PCA 4248 nor WEB 2170 suppressed the clinical signs of EAE. PAF concentration was measured in CNS tissue from the 9th day after inoculation to the 15th day, and no differences were found between control and EAE animals. These results suggest that PAF is not involved in the mediation of EAE.
 ...
PMID:Platelet-activating factor antagonists do not protect against the development of experimental autoimmune encephalomyelitis. 205 71


1 2 3 4 5 6 7 8 9 Next >>