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At least 19 recordsLinked to original sources
PubMed1979

Hyperacute experimental allergic encephalomyelitis in rhesus monkeys as a model of acute necrotizing hemorrhagic encephalomyelitis.

A comparative study of clinical and morphological findings in three fatal cases of acute necrotizing hemorrhagic encephalomyelitis (ANHE) and hyperacute experimental allergic encephalomyelitis (HEAE) in rhesus monkeys is reported. In all cases ANHE was characterized clinically by definite prodromal respiratory infection. The course was rapidly progressive with fatal termination. The salient histopathological changes were necrosis of blood vessels with plasma exudation and fibrin impregnation, hemorrhages and inflammatory reaction in the damaged cerebral tissue. Perivascular lymphoid histiocytic infiltration with glial proliferation was also noted in all cases. Numerous compound granular cells were found in one case. HEAE was detected in five rhesus monkeys immunized with homological spinal cord emulsion with complete Freund adjuvant. The illness was acute or subacute and the course was rapidly progressive with a fatal end. There was multiple necrosis of small blood vessels with plasma exudation, fibrin impregnation and massive neutrophila infiltration of the damaged brain tissue in all rhesus monkeys with HEAE. There was also widespread glial proliferation and numerous compound granular cells alongside with necrosis of blood vessels in the brain. These findings suggest that HEAE in rhesus monkeys can be viewed as an adequate model of ANHE.

Adolescent↗
PubMed1990

Monoclonal antibody to Theiler's murine encephalomyelitis virus defines a determinant on myelin and oligodendrocytes, and augments demyelination in experimental allergic encephalomyelitis.

Theiler's murine encephalomyelitis virus (TMEV) causes a chronic demyelinating disease in mice. The mechanisms underlying the demyelination have not been fully elucidated. We have raised a mAb to TMEV (DA strain), H8, that reacts both with TMEV VP-1 and galactocerebroside (GC). In mouse brain cultures, cells positive for the mAb H8 epitope were double labeled with antibody to myelin basic protein, indicating that those cells were oligodendrocytes. Further, mAb H8 could immunostain myelin structures in frozen sections from mouse brains. When injected intravenously into mice with acute allergic encephalomyelitis, mAb H8 increased by 10-fold the size of demyelinated areas within the spinal cords. This is the first report demonstrating that an antibody to virus can enhance demyelination of a central nervous system disease. Ig fractions from the sera of mice with chronic TMEV infection had antibody(s) to GC, as well as to TMEV, as determined by ELISA. Furthermore, a competition ELISA for TMEV or GC antigen revealed that sera from these infected mice contained antibody(s) with the same specificity as mAb H8. Our results indicate that antibodies generated by immune response to TMEV can react with myelin and oligodendrocytes, and contribute to demyelination through an immune process.

Animals↗
PubMed1976

Porcine encephalomyelitis caused by hemagglutinating encephalomyelitis virus.

Six epizootics of encephalomyeltis in suckling pigs in Minnesota were attributed to infection with hemagglutinating encephalomyelitis virus. The disease occurred in 74 litters of pigs and was characterized by sudden onset of tremors, inappetence, weakness, atazia, and hyperesthesia, with high morbidity and case fatality rate. Pathologic changes consisted of marked nonsuppurative, nondemyelinating encephalomyelitis characterized by perivascular mononuclear cuffing, gliosis, neuronal death, and satellitosis. Clinical disease was limited principally to suckling pigs during a single farrowing period and did not recur in the herds involved during the ensuing 18 months.

Animals↗
PubMed1975

Anti-synaptic antibody in allergic encephalomyelitis. II. The synapse-blocking effects in tissue culture of demyelinating sera from experimental allergic encephalomyelitis.

It has been suggested that demyelination cannot account for all of the observed clinical symptoms of multiple sclerosis (MS), in particular the rapidity of onset and remission of the disease, and attention has been focussed on the role of the synapse in 'demyelinating diseases'. In the present paper we have attempted to resolve the fundamental question of the site of action of a demyelinating disease, experimental allergic encephalomyelitis (EAE), by the use of cultures of neonatal rat cerebellum. Electrophysiological and morphological development in these cultures run hand-in-hand, and in the first few days in vitro there is a 4-5 day period when synapses are both seen ultrastructurally and known to be functioning but before the onset of myelination. The serum from guinea pigs with EAE was added to these cultures at different stages during their development and the morphological and electrophysiological effects observed. An abolitionary effect on the bioelectric activity of the culture was only observed when the serum was added to mature, myelinated cultures. Also the same active sera had no effect on synaptic activity before myelination had occurred. We conclude that the synaptic blocking effect occurs only when myelin is destroyed.

Animals↗
PubMed1979

[Correlation of heredity and environmental factors in the etiology of Vilyui encephalomyelitis. II. A population genetic study in districts of Vilyui encephalomyelitis distribution].

Population-genetic investigation was carried out in the regions endemic for Viljuisk encephalomyelitis (VE). The following indices were estimated: the relationship coefficient, the inbreeding coefficient, the intensity of migration, genetic structure of the population. The aim of the investigation was to explain causes of intrapopulational and, in some cases, of intragenus accumulation of the VE patients. No evidence of isolation or increased inbreeding were found in highly affected populations. The genetic structure of a group of VE patients tested for 9 polymorphic systems did not reveal any deviation from the control group. Several VE cases in healthy populations occured in some years after the immigration of a VE patient. These data confirm the hypothesis that VE is transmitted from a VE patient to healthy persons. Among these persons fall ill those who have a hereditary determined increased sensitivity to VE which results in intrapopulation and intragenus accumulation of VE cases.

Adult↗
PubMed1975

[Experimental allergic encephalomyelitis as a model for the study of therapeutic concepts for encephalomyelitis disseminata].

The induction of immunological tolerance with, and for, the caused organotypical antigen is a conception for a specific therapy for neuroimmunological diseases with at least a partial autoallergic pathogenesis. Appropriate to a set step-by-step programme for the development of antigen-specific therapy preventive tolerance experiments were carried out at the model of experimental allergic encephalomyelitis (EAEM) with allogenic myelin basic protein (BP) prepared from rabbits. The result is: 100 ug BP given intravenously simultaneously with 100 ug BP in incomplete Freud's adjuvant given intracutanously twice a week and 40 mg Cyclophosphamid given daily during the minor clinical incidence rate and no signs of EAEM pathomorphologically. A longlasting tolerance for the BP could be obtained as a test proved after 100 days. Hints are given for further potential therapeutic treatments, such as the use of antigen bound chemically to the immunosuppressive drug or the use of chemically modified BP for the induction of a specific tolerance.

Animals↗
PubMed1991

The role of prolactin in autoimmune demyelination: suppression of experimental allergic encephalomyelitis by bromocriptine.

Several lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory role on immune function and that pharmacological suppression of prolactin secretion with the dopamine-agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin-suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis-immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of sham-immunized rats. In vivo bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and was also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis.

Animals↗
PubMed1979

[Hyperacute encephalomyelitis following lyssa vaccination].

UNLABELLED: A case of hyperacute disseminated encephalomyelitis following lyssa-vaccination is reported. Clinical symptoms occurred on the tenth day after the vaccination and the patient died three days afterward. Demyelinization and glia proliferation was observed histologically in the spinal cord. No alterations could be seen in the peripheric nerves. CONCLUSIONS: 1. The spinal and cerebral forms of the postvaccinial encephalomyelitis can not be sharply distinguished. 2. In the postvaccinial encephalomyelitis there are also severe infiltration, demyelinization and gliosis in the opticus. 3. Post-vaccinial lyssa encephalomyelitis is a rare, but unavoidable complication of the lassa-vaccination. 4. The State Insurance Company have to pay damages.

Acute Disease↗
PubMed1991

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.

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.

Administration, Oral↗
PubMed1991

T-cell receptor peptide immunization leads to enhanced and chronic experimental allergic encephalomyelitis.

It has previously been reported that synthetic peptides corresponding to sequences derived from T-cell receptor variable regions identified as dominant in the T-cell-mediated autoimmune disease experimental allergic encephalomyelitis in both the mouse and the rat can down-regulate disease in Lewis rats. In contrast to these results, we have found that immunization of Lewis rats with such peptides in complete Freund's adjuvant prior to induction of experimental allergic encephalomyelitis with myelin basic protein leads to responses ranging from profound disease enhancement to lack of disease. In some cases, enhanced disease was followed by a prolonged neurologic deficit that resembles multiple sclerosis more closely than does acute experimental allergic encephalomyelitis. These findings, on the one hand, support previous results showing T-cell receptor peptide-induced modulation of the disease experimental allergic encephalomyelitis and, on the other, indicate that such immunization is not a reliable method for inducing suppression of encephalitogenic effector cells.

Amino Acid Sequence↗
PubMed1978

Post-infectious encephalomyelitis: some aetiological mechanisms.

The possibility that acute disseminated encephalomyelitis (ADEM) and epidemic myalgic encephalomyelitis ('epidemic neuromyasthenia') may share a common pathogenesis is examined and many factors common to the two diseases are described. It is suggested that further study of ADEM may help our understanding of epidemic myalgic encephalomyelitis.

Diagnosis, Differential↗
PubMed1979

Early events in canine distemper demyelinating encephalomyelitis.

The early neuropathological development of demyelinating Canine Distemper Encephalomyelitis (CDE) was studied in SPF dogs. Neural tissues were examined up to 30 days post infection (PI). Three phases of activity were observed. The primary event (first observed 8 days PI) was a nonsuppurative encephalomyelitis associated with the initiation of central nervous system (CNS) infection by virus-laden lymphocytes. At 24 days PI noninflammatory demyelination occurred in well defined, subependymal foci. Cell fusion and syncytia formation accompanied this early demyelination. The third phase, found at day 30 PI in one dog showing signs of recovery, was a second wave of nonsuppurative inflammation. The initial encephalomyelitis was widely disseminated throughout the CNS but subsequent demyelination appeared to be initiated from within the ventricular system. Myelin was phagocytosed by endogeneous CNS macrophages often infected with Canine Distemper Virus (CDV). The possible importance of viral induced cell fusion as well as immune factors in the mechanism of demyelination are discussed.

Animals↗
PubMed1991

Antigen-specific therapy of experimental allergic encephalomyelitis by soluble class II major histocompatibility complex-peptide complexes.

Experimental allergic encephalomyelitis is a T-cell-mediated, major histocompatibility complex (MHC) class II gene-linked autoimmune demyelinating disease of the central nervous system. To develop therapies that will specifically inactivate only the autoantigen-reactive T cells, mice were treated with soluble MHC class II molecules that had been complexed with encephalitogenic peptides. Intravenous injections of 300 micrograms of complexes consisting of encephalitogenic peptide 91-103 of myelin basic protein plus I-As protein on day 0, 4, and 7 were effective in preventing experimental allergic encephalomyelitis. Similarly, administration of 45 micrograms of I-As protein complexed to peptide 139-151 from proteolipoprotein on day 1, 4, and 7 prevented mortality and significantly reduced paralysis induced by immunization with the encephalitogenic proteolipoprotein peptide. Histological examination of sections of animal brains revealed that treatment with I-As protein plus myelin basic protein 91-103 peptide prevents the development of inflammatory lesions characteristic of experimental allergic encephalomyelitis. Thus, treatment with MHC-self-peptide complexes could serve as a highly specific therapeutic modality in treating autoimmune disease when the putative autoantigen and the MHC restricting elements are known.

Animals↗
PubMed1991

Accelerated response to reinoculation in experimental allergic encephalomyelitis: clinical study.

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.

Adjuvants, Immunologic↗
PubMed1977

Encephalomyelitis induced by canine distemper virus in non-human primates.

A strain of canine distemper virus was shown to be highly neuro-virulent in non-human primates. Intracerebral inoculation induced in monkeys histological lesions of encephalomyelitis, i.e., degenerative changes consisting mainly of neuronal damage and inflammatory changes such as perivascular cuffings and glial proliferation, in wide areas in the brain and spinal cord. In one monkey observed for 70 days, lesions with a tendency of subacute sclerosing were also noticed. Immunosuppression with cyclophosphamide or antithymocyte serum was found to aggravate the clinical course and to modify the histological lesions in the central nervous system as well as the level of antibody response to the virus in cerebrospinal fluid. Possible application of distemper encephalomyelitis in monkeys as a primate model for analysis of the immune mechanism involved in paramyxovirus-induced encephalomyelitis was discussed.

Animals↗
PubMed1976

[Comparative study of infectious and atypical encephalomyelitis in birds].

Studied were morphologically a total of 234 birds for infectious encephalomyelitis (IE) and atypic encephalomyelitis (AE) of which 70 were experimentally infected with standard reference strains of IE (Calnek 1143-42 birds, and Van Roeckel 28 birds), 32 were infected with a brain suspension of affected with AE birds, and 110 were spontaneously affected with AE. Those of the birds that were infected with the standard strains of IE as well as with the brain suspension exhibited changes in the central nervous system in the form of a non-suppurative encephalomyelitis, and in the viscera--lymphoidcell proliferations. These alterations proved analogous with those observed in birds spontaneously affected with AE. The changes in CNS in the case of IE were localized in the brain and the spinal cord, while the lesions in the case of AE were found chiefly in the brain. In AE there were perivascular lymphoidcell were groupings along the peripheral nerves. It was concluded that the histologic changes established may well serve to differentiate IE from AE in Marek's disease, the transitional paralysis, the Newcastle disease, and the alimentary encephalomalacia.

Animals↗
PubMed1979

[Immune complexes in multiple sclerosis and experimental allergic encephalomyelitis].

Immune complexes in the blood serum were determined in patients with disseminated sclerosis and in dogs in the process of experimental allergic encephalomyelitis. In disseminated sclerosis the existence of immune complexes was found in the exacerbation period and their absence in remissions. In animals with clinical signs of experimental allergic encephalomyelitis the immune complexes began to be established in the period of sensitization and attained the maximum in the preparalytic and paralytic period. In animals without clinical signs, the immune complexes were determined later and in insignificant amounts. The role of immune complexes in the pathogenesis of exacerbations in disseminated sclerosis and development of experimental allergic encephalomyelitis as factors involved in the disturbances of permeability in the hematoencephalic barrier is discussed.

Adrenalectomy↗
PubMed1975

The effect of specific brain phospholipid on the rat's allergic encephalomyelitis.

A new preparation which contains specific brain phospholipids (Gricertine) acts as a histamine liberator in CNS and protects rats from allergic encephalomyelitis. It is supposed that the protective effect of Gricertine on the allergic encephalomyelitis is based on its histamine-liberator properties which can occur during the first days of therapy: this would explain the large decrease of the brain histamine after 3 weeks of treatment. Gricertine is also able to remove clinical symptoms of allergic encephalomyelitis in rats. It is presumed that Gricertine may also be acting independently of that mechanism, in the way that it replaces phospholipids that disappeared in the cases where demyelinisation had taken place.

Animals↗