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At least 19 recordsLinked to original sources
PubMed1975

Experimental allergic encephalomyelitis (EAE) in mice. I. Induction of EAE with mouse spinal cord homogenate and myelin basic protein.

The condition of experimental allergic encephalomyelitis (EAE) induction was investigated in several mice strains. SJL and C3H/He strains were found to be susceptible. A single immunization with mouse spinal cord, complete Freund's adjuvant (CFA) and pertussis vaccine produced clinical signs of EAE in SJL and C3H/He strains after 11 to 18 days. Isogenic spinal cord produced EAE in C3H/He strain. A single immunization with myelin basic protein from bovine spinal cord in CFA and pertussis vaccine produced EAE in SJL strain. EAE susceptibility of SJL strain correlated with the amount of mycobacteria used for sensitization. It was necessary to give pertussis vaccine intravenously in all cases.

Animals↗
PubMed1976

Experimental allergic encephalitis (EAE) in mice: histological studies on EAE induced by myelin basic protein, and role of pertussis vaccine.

The histological evidence of EAE in mice was presented to show the identity with those of other species of animals. There was a typical perivascular mononuclear cell infiltration. In addition, a hyperacute form was characterized by edema and the infiltration of polymorphs. In vascular lesions, vascular stasis, thrombosis, and hemorrhage were observed. As for the effect of pertussis vaccine used in the induction of mouse EAE, responsiveness to the histamine sensitizing factor was not directly correlated to the incidence of EAE. However, the intravenous administration of pertussis vaccine caused remarkable leukocytosis, which might play a certain role in mouse EAE induction.

Animals↗
PubMed1977

Herpes simplex infection and experimental allergic encephalomyelitis. An experimental model system for reactivation of EAE.

The effects of herpes simplex virus type 1 (HSV-1) infection on the course of experimental allergic encephalomyelitis (EAE) were studied in rats. Fifty percent of animals given two intracerebral injections of HSV-1, one before and one after induction of EAE, showed clinical and pathologic evidence of recently exacerbated EAE 16 days after the second HSV-1 injection. When HSV-1 injections were administered subcutaneously before and after induction of EAE, 45% of survivors showed pathologic changes of recent EAE. A single injection intracerebally or subcutaneously of HSV-1 given before the development of EAE did not change the clinical severity or time course of EAE. A single injection intracerebrally or subcutaneously of HSV-1 given after the development of EAE did not cause clinical recrudescence of the EAE. Pathologic but not clinical evidence of EAE recurrence was found in three of nine animals given one injection of HSV-1 intracerebrally before and one of control material intracerebrally after induction of EAE. Pathologic evidence of EAE recurrence was found in six of 14 rats given one injection of control material intracerebrally before and one of HSV-1 intracebrally after induction of EAE. Cell suspensions, free of HSV-1, given prior and subsequent to the development of EAE did not cause a change in the EAE severity or a recrudescence of the EAE.

Animals↗
PubMed1976

Improvements for consistently inducing experimental allergic encephalomyelitis (EAE) in rats: I. without using mycobacterium. II. inoculating encephalitogen into the ear.

Several methods of inducing experimental allergic encephalomyelitis (EAE) in rats were examined using different (i) rat strains, (ii) combinations of encephalitogen with different adjuvants, and (iii) sites of encephalitogen inoculation. The time course and severity of the ensuing diseases were determined and methods delineated for inducing a disease with limited variability and high incidence. Omitting the mycobacterial component from the adjuvant eliminated the complication of adjuvant arthritis, which may develop after the appearance of EAE. Encephalitogenic emulsions prepared with an equal volume of frozen guinea pig spinal cord (GPSC) and hexadecane or squalene, injected into two inguinal nodes or one foot pad of Lewis rats, provided two quick and easy ways to induce EAE. Emulsions of encephalitogen with Freund's complete adjuvant or hexadecane, injected into the ear, also induced EAE but lengthened the time between the antigen inoculation and clinical symptoms which accompany the onset of EAE disease. However, injection into the ear offers an advantage over the Newbould technique (direct instillation of encaphalitogen in pre-exposed lymph nodes), since the animals can be confidently predosed with drugs which may reduce lymphoid mass. Effects of local inflammation on systemic drug metabolism are also minimized when using the ear route.

Adjuvants, Immunologic↗
PubMed1979

Effect of cyclophosphamide on suppressor cell activity in mice unresponsive to EAE.

Protection against experimental allergic encephalomyelitis (EAE) was induced in susceptible mice of (SJL/J X BALB/c)F1 hybrid, by injection of either mouse spinal cord homogenate, the small mouse basic protein, or Cop 1 in incomplete Freund's adjuvant, before EAE induction. It was demonstrated that the unresponsiveness induced by the three antigens is mediated by suppressor T cells residing in the spleen cell population and can be adoptively transferred to normal syngeneic recipients. Low dose of cyclophosphamide (20 mg/kg) administered 2 days before the encephalitogenic challenge abrogated the unresponsiveness to EAE and reverted the protected mice sensitive to disease induction. Cyclophosphamide was also active on adoptively transferred unresponsiveness, thus donors that had been treated with cyclophosphamide were unable to further transfer unresponsiveness to EAE. These results indicate the elimination by cyclophosphamide of suppressor cells that interfere with the effector mechanisms leading to EAE.

Animals↗
PubMed1978

Clearance of myelin basic protein from blood of normal and EAE rabbits.

The rate of clearance of porcine myelin basic protein (MBP) from plasma of rabbits was determined following intravenous injection of 20 mg MBP. The MBP level in the plasma was measured by a 2-site immunoradiometric assay with specific antibody to guinea pig MBP produced in rabbits. Plasma MBP-antibody levels were determined by competitive binding radioimmune assay (RIA). Unsensitized and those sensitized with complete Freund's adjuvant (CFA), with porcine MBP in CFA, and with whole porcine spinal cord in CFA were studied. Unsensitized and CFA sensitized rabbits exhibited maximum MBP levels in the plasma within two minutes after injection with rapid decrease to undetectable levels in one hour. Thirty-nine of the unsensitized (control) rabbits exhibited normal, rapid clearance and no subsequent physical signs of EAE while one of the control rabbits exhibited a slightly retarded clearance rate. Histologic examination of autopsy tissues from the control group revealed that five rabbits showed lesions which could be attributed to Encephalitozoan cuniculi or Toxoplasma and one rabbit autopsied 65 days after clearance had minimal EAE lesions. Rabbits sensitized with MBP exhibited a retarded rate of clearance at the acute stage of EAE and following recovery. Rabbits sensitized with whole spinal cord in CFA also exhibited a retarded rate of MBP clearance. Anti (MBP) antibodies were detected in the plasma of all rabbits which exhibited a retarded rate of MBP clearance. Significant rates of retardation were not detected until approximately three weeks after sensitization with CFA-MBP or CFA-spinal cord. While MBP antibody levels in most animals were not detected by the immunodiffusion technique, antibodies were demonstrated by RIA. The 20 mg MBP given intravenously is probably in great antigen excess and conducive to the formation of soluble MBP-anti (MBP) complexes in the blood.

Animals↗
PubMed1975

Adoptive transfer of experimental allergic encephalomyelitis (EAE): prevention of successful transfer by treatment of donors with myelin basic protein.

After onset of experimental allergic encephalomyelitis (EAE), guinea pigs can be effectively treated by injection with myelin basic protein (BP). In order to localize the site of action of BP, cells from sensitized donors treated with BP one, two, three, or four times after disease onset have been transferred to normal recipients. One injection of BP has no effect on ability of cells to transfer EAE. Two injections partially inhibit transfer. After the third and fourth injections the sensitized cells lose their capacity to transfer EAE. The therapeutic effect of BP previously demonstrated in actively sensitized guinea pigs must involve the specifically sensitized cells rather than the target organ.

Animals↗
PubMed1979

Decrease in motor activity - an early symptom in the course of experimental allergic encephalomyelitis (EAE).

Motor activity has been followed in rats during an experimental allergic encephalomyelitis (EAE). The disease was produced by transfer of lymph node cells from sensitized syngenic donors. Small and large movements were permanently registered by an electric activity meter. It could be demonstrated that a decrease of the motility is an early symptome of the disease. Therefore the measurement of the motoric activity might be a useful parameter in the classification of EAE.

Animals↗
PubMed1976

Modifications in the establishment of allergic encephalomyelitis (EAE) in rats; an imporved assay for immunosuppressant drugs.

EAE induced in Lewis rats by guinea-pig spinal cord and such lipid adjuvants as hexadecane or squalene (without the mycobacterial component) is more sensitive to lower doses of cyclophosphamide and some select immunosuppressive agents than the conventional EAE induced using Freund's complete adjuvant. In addition, these animals do not suffer from adjuvant arthritis which may be induced if the bacterial component is present. These modifications in the conventional assay have enhanced its ability to detect new, weaker and/or lower doses of known immunosuppressants.

Adjuvants, Immunologic↗
PubMed1977

Characterization of the in vitro cytotoxic assay of immune lymphoid cells in experimental allergic encephalomyelitis (EAE).

Complement, antilymphocyte globulin, antiencephalitogenic antigen serum, actinomycin D and mitomycin C inhibited the cytotoxicty against syngenic fibroblasts of spleen cells more than lymph node cells. The results strongly suggest that the immune cell populations in EAE in the spleen andlymph nodes are qualitatively and/or quantitatively different. Cytotoxicity was dependent upon the number of immnue cells in the test. There was evidence of antigenic competition between encephalitogenic antigen and Myocobacterium tuberculosis in the induction of EAE.

Animals↗
PubMed1978

2 [(methylsulfinyl) acetyl] pyridine (Oxisuran): a new immunosuppressive agent in EAE.

The authors discuss the effects of a new immunosuppressive agent on the development of EAE. Animals (albino rabbits) were inoculated with an encephalitogenic emulsion, according to Kies' method, whereas a control group was inoculated by a physiological saline solution. Some animals were treated by Oxisuran in the first day after challenge; some others after initial symptoms (18th day). Thirty days after challenge, the animals were sacrificed. No toxicity was found in thoracic and abdominal structures neither in blood count. Pharmacological effectiveness of Oxisuran is well documented either in pretreatment or in therapy; the course was positively influenced in animals, when treated after the appearance of initial symptoms.

Animals↗