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)

Adjuvant arthritis is induced by intradermal injection of Mycobacterium tuberculosis (MT) in oil. The role of immunity to type II collagen (CII) in adjuvant arthritis (AA) has not been well defined. We found that oral administration of chicken CII given 3 micrograms per feeding on days -7, -5, and -2 before disease induction consistently suppressed the development of AA. A decrease in delayed-type hypersensitivity responses to CII was also observed that correlated with suppression of AA. AA was optimally suppressed by 3 and 30 micrograms of collagen type II variably by 300 micrograms, and not by 0.3 microgram or 1 mg. Oral administration of collagen type I also suppressed AA; only minimal effects were seen with collagen type III. Suppression was Ag specific: feeding CII did not suppress experimental autoimmune encephalomyelitis; feeding myelin basic protein suppressed experimental autoimmune encephalomyelitis, but not AA. Suppression of AA could not be consistently obtained by feeding MT. Suppression of AA could be adoptively transferred by T cells from CII fed animals and could be obtained when CII was fed after disease onset. Our results suggest that autoimmunity to CII has a pathogenic role in AA and raise the possibility that cross-reactive epitopes exist between CII and MT. Alternatively, the pathogenesis of AA may be dependent on developing immunity to CII. These results further demonstrate the effectiveness of oral tolerance as a means to suppress experimental autoimmune diseases.
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PMID:Suppression of adjuvant arthritis in Lewis rats by oral administration of type II collagen. 212 Mar 32

In strain-13 guinea-pigs inoculated for chronic relapsing experimental allergic encephalomyelitis (CR-EAE), IgG1 and IgG2 subclass antibody responses were investigated using single radial immunodiffusion and enzyme-linked immunosorbent assays (ELISA) for IgG1 and IgG2 specific for whole cord, myelin, myelin basic protein and Mycobacterium tuberculosis. The early acute stage revealed no increase in IgG1 but was associated with increased levels of IgG2 specific for neural and adjuvant components. Throughout the chronic phase of the disease, there were increased levels of IgG of both subclasses specific for the antigens tested but a preferential synthesis of IgG1. Levels of both IgG1 and IgG2 specific for neuroantigens were lowest in those guinea-pigs which did not develop signs of chronic disease. Immediate skin sensitivity against a wide range of neural antigens was not demonstrated though positive results may have been masked by the ability of myelin basic protein to induce non-specific mast cell degranulation and by altered histamine responsiveness in disease. Guinea-pigs with chronic paralysis had a lower skin sensitivity to histamine, compound 48/80 and M. tuberculosis than those in remission.
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PMID:IgG subclass responses and immediate skin sensitivity in guinea-pigs with chronic relapsing experimental allergic encephalomyelitis. 244 54

Dark August rats exhibit clinically and histologically verified experimental allergic encephalomyelitis (EAE) when immunized with appropriate antigen (nervous tissue, myelin basic protein) emulsified in complete Freund's adjuvant (CFA). We provide evidence that 6,6'-trechalose dymicolate (TDM) incorporated in incomplete Freund's adjuvant replaces CFA in EAE induction. The animals that recovered from EAE were resistant to the reinduction of the disease irrespectively whether Mycobacterium tuberculosis or TDM was used as an adjuvant. Finally, pretreatment with CFA alone was sufficient for prevention of disease elicited by challenge with encephalitogen + CFA. However, TDM, despite its adjuvant capacity when applied prior to the induction of the disease with encephalitogen + CFA, did not exhibit any protective effect. Thus, our study implicates that adjuvant and suppressive capacities of M. tuberculosis may be related to the different determinants of the microorganisms, TDM possessing the adjuvanticity only.
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PMID:Dissection of adjuvant and suppressive effects of mycobacteria in experimental allergic encephalomyelitis production. 244 46

We report the use of the ELISA technique to measure IgG specific for whole cord, myelin, myelin basic protein and Mycobacterium tuberculosis in the cerebrospinal fluid (CSF) of Strain 13 guinea pigs in different stages of chronic relapsing experimental allergic encephalomyelitis (CR-EAE). Specific antibody levels to all 4 antigen preparations were related to the severity of clinical signs, with the highest levels of IgG in the CSF of guinea pigs in relapse or in stable chronic disease. Total IgG levels in the CSF, though elevated throughout the course of CR-EAE, did not show any association with the category of disease. Control animals inoculated with complete Freund's adjuvant (CFA) alone showed CSF IgG levels specific for M. tuberculosis that were not significantly different from those in animals with chronic EAE, indicating that CFA may itself induce a late-acting increase in blood-brain barrier permeability.
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PMID:Autoantibody responses in the cerebrospinal fluid of guinea pigs with chronic relapsing experimental allergic encephalomyelitis. 246 68

The source of IgG in the cerebrospinal fluid (CSF) in guinea pigs with chronic relapsing experimental allergic encephalomyelitis (CR-EAE) was investigated using quotient analysis of total IgG and albumin concentrations and by computing CSF-plasma ratios of specific IgG concentrations. Increased blood-CSF barrier (B-CSFB) permeability was shown by elevated albumin quotients in both relapse and remission phases of CR-EAE and intrathecal production of IgG was indicated by raised ratios of IgG to albumin in the CSF. Intrathecal IgG synthesis was greatest in guinea pigs which had little B-CSFB damage. When enzyme-linked immunosorbent assays (ELISA) for whole cord, myelin basic protein (MBP) or Mycobacterium tuberculosis were performed with CSF and plasma adjusted to the concentration of total IgG, the CSF/plasma ratios of ELISA results for specific antibodies were less then unity and ratios for whole cord and MBP were lower than those for M. tuberculosis. There was thus no evidence for a selective increase in the CSF of antibody specific either for the neuroantigens tested or for adjuvant components. The CSF-plasma ratios for each specific antibody were inversely correlated with the extent of total IgG intrathecal synthesis, suggesting that much of the antibody production within the CNS is the result of polyclonal B cell activation.
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PMID:The origin and specificity of intrathecal IgG in chronic relapsing experimental allergic encephalomyelitis. 248 78

A single injection of complete Freund's adjuvant blended with aluminum hydroxide gel (ALU-CFA) was successfully used to prevent clinical as well as histologic experimental allergic encephalomyelitis (EAE) in Lewis rats for more than 330 days. Adjuvant preparations with Mycobacterium tuberculosis were more potent than those with Mycobacterium butyricum. Neither the removal of the ALU-CFA inoculum nor a splenectomy 1 month after immunization arrested the adjuvant induced unresponsiveness. However cyclophosphamide restored responsiveness in more than half of the treated animals when applied 2 days before the encephalitogenic challenge at a dose of 20 mg/kg. Passive EAE was not prevented by the ALU-CFA pretreatment. The disease was induced by the transfer of 4 X 10(6) T lymphocytes of a cell line reactive against myelin basic protein. This indicates that the adjuvant prevents EAE at the inductive rather than at the effector phase of the autoimmune response.
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PMID:Unresponsiveness to experimental allergic encephalomyelitis in Lewis rats pretreated with complete Freund's adjuvant. 257 28

Previous work from this laboratory has shown that resistance to acute experimental autoimmune encephalomyelitis (EAE) correlates with disease-specific, antigen-induced suppression of blastogenesis in vitro. We now report that this suppression in vitro also occurs during remissions in animals with chronic-relapsing EAE. Hartley strain guinea pigs were injected with an homogenate of guinea pig spinal cord in complete Freund's adjuvant (CFA) to induce EAE or, for control purposes, with CFA alone. Animals injected with spinal cord homogenate developed EAE. Susceptible animals displayed up to 3 exacerbations over 4-5 months. Spleen cells and nervous tissue were sampled from different animals during and after each exacerbation. Gross examination of nervous tissue revealed plaques that at the light microscope level were characteristic of chronic-relapsing EAE. Lymphocyte transformation assays using the T-cell mitogen concanavalin A (Con A), guinea pig myelin basic protein (BP), the purified protein derivative of M. tuberculosis (PPD) and histone proteins were conducted. Results of these assays showed that in spleen cells from animals sampled during remissions, BP suppressed the Con A response. Similar suppression was not observed with spleen cells from animals in exacerbation. This suppression depended upon the presence of adherent cells. Neither PPD nor histone proteins suppressed the Con A response. Thus, an immunologic mechanism, similar to that observed in Hartley guinea pigs resistant to acute EAE, is also found during remissions in the chronic-relapsing form of this disease suggesting that both resistance and remission are mediated by an antigen-induced suppressor mechanism.
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PMID:Chronic-relapsing experimental autoimmune encephalomyelitis. Myelin basic protein induces suppression of blastogenesis during remissions but not during exacerbations. 257 93

Acute experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats by inoculation with guinea pig spinal cord homogenate emulsified with Mycobacterium tuberculosis-enriched complete Freund's adjuvant (CFA). Control rats were inoculated with CFA alone. Control and EAE rats were killed on days 7, 9, 11, and 13 postinoculation, and regional brain and spinal cord levels of histamine were determined. No regional differences in histamine content between control and EAE rats were seen on day 7 or 9 postinoculation. However, depending on the region, EAE rats exhibited significantly higher levels of histamine in their CNS on day 11 or 13 postinoculation or on both. Thus, regionally and temporally specific increases in brain and spinal cord levels of histamine develop concomitant with or just after the appearance (on day 10 postinoculation) of clinical signs of acute EAE, a finding suggesting that histamine may be involved in the development or expression of acute EAE in Lewis rats.
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PMID:Brain and spinal cord levels of histamine in Lewis rats with acute experimental autoimmune encephalomyelitis. 278 54

Different forms of experimental allergic encephalomyelitis were obtained in 4 groups of guinea pigs: 7 adult Hartley guinea pigs (Group I), 12 adults of the same strain (Group II), 6 juvenile strain 2 guinea pigs (Group III) and 6 juvenile strain 13 animals (Group IV), by the injection of emulsions. Groups I and II received emulsions containing 250 mg and 500 mg respectively of fresh isologous spinal cord tissue, complete Freund adjuvant (CFA) and saline solution while Groups III and IV received an emulsion containing 120 mg of isologous spinal cord, CFA, saline solution and 15 mg of Mycobacterium tuberculosis. The increased antigen load induced a disease with delayed onset and prolonged progressive course (C-P-EAE) in Groups I and II, although 8 animals showed no symptoms of illness. The findings in C-P-EAE were large demyelinated plaques, perivenous fibrosis and large areas of infiltration. Demyelinated areas occurred within the spinal cord white matter only in two asymptomatic animals. C-P-EAE was obtained in 4 of the Strain 2 animals. In conclusion, the increased antigen load induced a range of lesions in Hartley guinea pigs, although not all animals were affected. C-P-EAE was induced also in strains of guinea pig other than the Heartley strain. These different reactions may have been the outcome of partial or complete inactivation of the cell-mediated response to the inoculated antigens.
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PMID:Experimental allergic encephalomyelitis in guinea pig: variability of response to intradermal emulsion injection. 292 44

Chronic relapsing experimental allergic encephalomyelitis (CR-EAE) was induced in rats with an emulsion of guinea-pig spinal cord tissue (GPSC) in complete Freund's adjuvant (CFA) enriched with Mycobacterium tuberculosis H37RA (Tbc). 78% of the sensitized rats developed a CR-EAE showing 2 to 3 clinical relapses during the first 40 days. After 60-80 days, approximately half of the rats with CR-EAE had a further relapse which was followed by complete recovery in only 35% of the cases. The remaining 65% of these animals showed a progressive state of the disease, characterized by paralysis or severe motor deficit, eventually leading to death. CR-EAE in rats showed some similarities to multiple sclerosis in man (MS) and it may be a useful model for the study of this disease.
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PMID:Chronic relapsing experimental allergic encephalomyelitis in the Lewis rat. 387 41


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