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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral administration of 2, 3 or 4 doses of 100 or 250 mg/kg of EN3638 during the incubation period of experimental allergic encephalomyelitis delayed the onset and reduced the incidence and severity of clinical signs and histological lesions. Five doses of 50 or 100 mg/kg effected virtually complete and permanent suppression of clinical signs even after cessation of therapy, and five doses of 250 mg/kg eliminated histological lesions as well. Optimum results required coverage of the entire incubation period regardless of dose level. These results were obtained only when carbonyl iron was used as the adjuvant for production of EAE. When complete Freund's adjuvant was used, EN3638 delayed the onset but had little or no influence on late-developing clinical signs and histologic lesions after cessation of therapy. The permanence of suppression when carbonyl iron was used is related to the absence of an oil depot. Carbonyl iron is a superior adjuvant for drug suppression studies.
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PMID:Suppression of experimental allergic encephalomyelitis by EN3638: dependence on adjuvants and treatment schedules. 40 21

Brown Norway (BN) rats are much less susceptible to experimental allergic encephalomyelitis (EAE) than Lewis rats. Nevertheless, BN rats developed severe EAE, even paralysis, when immunized with rat spinal cord and carbonyl iron adjuvant. Complete Freund's adjuvant (CFA) was much less effective. The use of both CFA and pertussis vaccine with rat cord was moderately, but not consistently, effective. Guinea pig spinal cord was weakly encephalitogenic to BN rats with all adjuvant combinations. We were not able to produce EAE in BN rats with purified myelin basic protein from either rat or guinea pig. Inoculations directly into lymph nodes or into the blood stream proved that the low susceptibility of BN rats was not due to lack of absorption from the site of inoculation, but may be related to peculiarities of processing antigen in draining lymph nodes. The severity of EAE in F1 hybrids was intermediate between the BN and Lewis parental strains when tested with an immunizing procedure of appropriate strength. The fact that F1 hybrids were less reactive than Lewis mandates modification of the theory that susceptibility to EAE is inherited through a single autosomal dominant gene.
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PMID:Allergic encephalomyelitis in the reputedly resistant Brown Norway strain of rats. 112 Sep 1

Experimental allergic encephalomyelitis (EAE) was induced in Lewis rats by the injection of spinal cord tissue or myelin basic protein and adjuvants (Freund's or carbonyl iron or pertussis vaccine), or by adoptive immunization. After an interval of five to 12 weeks, the recovered rats were reinoculated by a different route and usually with a different adjuvant. The onset of the second attack was determined by the histologic detection of EAE lesions at intervals during the incubation period. In each of ten experiments, the second attack of EAE occurred one or two days earlier than in naive controls injected at the same time. Residual EAE lesions left over from the first attack could not explain the findings in the reinoculated rats. The accelerated response to the second inoculation may be related to the anamnestic response of classical immunology or to residual damage to the blood-brain barrier. Resistance to a second attack was not encountered in this histopathologic study.
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PMID:Accelerated response to reinoculation in experimental allergic encephalomyelitis: histopathologic study. 170 89

An attack of experimental allergic encephalomyelitis is generally thought to confer resistance to a second attack. Nevertheless, some authors have produced second attacks, sometimes with an anamnestic shortening of the incubation period. In addition, second attacks of experimental allergic encephalomyelitis with accelerated onsets following reinoculation were found in every experiment when histopathologic rather than clinical criteria were employed. In the present work, we found that clinical signs with accelerated onset were also found in each experiment provided that the first attack was produced with the aid of Freund's complete adjuvant and provided that the reinoculation stimulus was the highly potent combination of rat spinal cord and carbonyl iron. Whatever the potency of the reinoculation, and regardless of the occurrence of an accelerated onset, the eventual outcome was a decreased severity and mortality of the second attack of experimental allergic encephalomyelitis. The new data demonstrate that accelerated onset is not necessarily an indication of increased severity.
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PMID:Accelerated response to reinoculation in experimental allergic encephalomyelitis: clinical study. 180 98

Magnetic fields (MF) can influence biological systems in a wide range of animal species and humans. We report here on the influence of static MF, locally applied to the brain area, on immune system performances in the rat. In the first series of experiments two AKMA micromagnets (M) with the influx density of 600 Gauss were bilaterally implanted (with "N" polarity facing the cranial bones) and fixed to the skull posterior to the fronto-parietal suture (parietal brain exposure). Rats implanted with iron beads (I) and sham-operated (SO) rats served as controls. Animals were exposed to MF or I during different periods of time before and after immunization with several soluble or cellular antigens. We report here on the in vivo immunoregulating effects of centrally applied MF on plaque-forming cell (PFC) response, local hypersensitivity skin reactions and experimental allergic encephalomyelitis. The selective influence of MF applied to different brain regions on PFC response was evaluated, as well. For this purpose, two M were bilaterally implanted in the area of (a) frontal, (b) parietal and (c) occipital brain regions. Rats were under the influence of MF for 20 days before and 4 days after immunization with sheep red blood cells. Groups of nonimmunized rats were exposed for 14, 24 and 34 days to parietally implanted M or I, and the number of peripheral blood CD4+ and CD8+ cells determined by mouse anti-rat W3/25 and MRC OX 8 monoclonal antibodies. The results show an overall in vivo immunopotentiation of humoral and cell-mediated immune responses in rats exposed to MF. Furthermore, these immunomodulating effects of centrally applied MF depend on at least two basic parameters, time of exposure and brain region exposed. The highest immune performance was obtained after exposure of the occipital brain region for a total period of 24 days. The results provide further evidence of the complex interrelationship between the environment, the central nervous system and the immune system.
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PMID:Magnetic fields, brain and immunity: effect on humoral and cell-mediated immune responses. 183 91

Induction of experimental allergic encephalomyelitis (EAE) in Lewis rats by injection of guinea pig (GP) spinal cord homogenate (SCH) plus adjuvant (SCH-CFA) can be inhibited by treatment with the iron chelating agent desferrioxamine (DFOM). Interestingly, induction of EAE with purified myelin basic protein (BP-CFA) is not inhibited with DFOM. This dichotomy does not appear to be due to any quantitative differences in the two inocula since minimal clinical EAE produced by threshold levels of BP is not inhibited with DFOM. Passive EAE is not inhibited irrespective of the type of encephalitogen used to sensitize the donors. This suggests that the inhibitory effect of DFOM is acting on the afferent limb of the immune response to SCH-CFA. Injection of BP-CFA and SCH-CFA into the same site, mixing BP with central nervous system (CNS) lipids, or incorporating BP into liposomes, all induce EAE which can be partially inhibited by treatment with DFOM. These results support the hypothesis that the close association of lipids with the encephalitogen (i.e. BP) in SCH required extensive lipid breakdown before adequate antigen presentation can occur, and it is at this level that DFOM exerts its inhibitory effect.
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PMID:Inhibition of allergic encephalomyelitis by the iron chelating agent desferrioxamine: differential effect depending on type of sensitizing encephalitogen. 244 24

The designation of Brown-Norway (BN) rats as resistant to experimental allergic encephalomyelitis (EAE) is an oversimplification. Lewis rats are susceptible and BN rats are usually resistant to EAE after inoculation with guinea pig spinal cord or basic protein in Freund's adjuvant. However, EAE can be produced in BN rats by immunizing with rat cord and carbonyl iron, a particulate adjuvant. In the present work, the possibility that susceptibility of BN rats under these conditions is due only to the special qualities of the adjuvant has been eliminated by producing EAE in them without any adjuvant at all, merely by increasing the absorption and processing of the rat cord antigen. The susceptibility of the F1 hybrids is intermediate with respect to guinea pig cord antigen but it was equal to or greater than either parental strain when tested with rat cord antigen. Histologic evidence that BN rats do not absorb or process neural antigen as well as other strains, and the augmentation of EAE by increasing the dose and absorption of the inoculum, suggest that antigen absorption, processing and presentation is a "bottleneck" for development of EAE in BN rats. Absorption and processing of antigen should be considered along with cellular response, inflammatory mediators and epitope dominance when analyzing susceptibility and resistance to EAE.
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PMID:The role of antigen absorption in the resistance of brown-Norway rats to experimental allergic encephalomyelitis. 246 73

The hyperacute form of experimental allergic encephalomyelitis (EAE), characterized by a short incubation period, severe paralysis, high mortality, and abundant polymorphonuclear leukocytes and fibrin in the lesions, was produced in rats without the use of pertussis vaccine (previously considered an essential requirement) or Freund's adjuvant. Carbonyl iron or mineral oil without mycobacteria were effective adjuvants and whole rat spinal cord was the best antigen. Hyperacute EAE was produced in this manner in some Lewis rats, most dark agouti (DA) rats and most F1 hybrids of these two strains. Clinical signs were earlier in onset and more severe in the DA strain than in the Lewis strain in all adjuvant-antigen combinations that were tested. Dark agouti rats developed clinical signs in six days, histological lesions in five days, and localized EAE lesions could be induced in four days. The data support the hypothesis that hyperacute type lesions (neutrophils and fibrin) can be caused by an exceptionally strong immune response to neural antigen, whether that response is engendered by a particular adjuvant (pertussis vaccine) or by an unusual degree of genetic susceptibility (DA rats).
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PMID:The hyperacute form of allergic encephalomyelitis produced in rats without the aid of pertussis vaccine. 278 30

Large intravenous doses of a relatively nontoxic iron polymaltose complex were taken up by liver and spleen and did not enter the central nervous system (CNS) of normal rats. When the injections were given during development of the inflammatory lesions of experimental allergic encephalomyelitis (EAE), many iron-laden macrophages entered vessels, perivascular cuffs and neural parenchyma. Iron polymaltose injected before the EAE lesions started to develop, or during the healing phase, did not enter the lesions. This model of CNS siderosis may be useful for studies on long-term effects of iron and for neuroimaging by nuclear magnetic resonance.
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PMID:Inflammatory siderosis of the nervous system in rats. 278 55

Carbonyl iron and several other particulate materials have been reported to enhance the development of experimental allergic encephalomyelitis when injected with neural antigen. In the present work, silicon and silica powders have been added to the list of particulate adjuvants. In addition, several particulate materials, but not carbonyl iron, were effective adjuvants when inoculated four weeks or even six months before the neural antigen. It was necessary for adjuvant and antigen to be injected in the same region, but both intraperitoneal and subcutaneous routes were effective. The long-lasting adjuvanticity of certain particulates in the tissues is probably related to their bland and unabsorbable nature. The reasons for restrictions in the range of adjuvants and antigens that are effective in this system and the possibility of a similar occurrence in nature remain to be investigated.
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PMID:Enhancement of allergic encephalomyelitis by particulate adjuvants inoculated long before antigen. 624 3


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