Histochemistry of oxidative enzymes in experimental allergic encephalomyelitis.

The histoenzymic pattern of oxidative enzymes (G3PD, IDH, SD, G6PD,HBD, NADPH: dehydrogenase) was investigated in experimental allergic encephalomyelitis (EAE) produced in rats according to PATERSON [13]. The results obtained lead to following conclusions: (1) The neuroglia, including the white matter oligodendroglia of immunized rats, exhibits increased oxidoreductase activities; (2) The neuroallergic reaction induces some stimulation of the oxidoreductive metabolism of oligoden-droglia; (3) The enzymatic hyperactivity in EAE does not show any relation to the morphological signs of alterations of the myelin sheath.     

Correlation of cytotoxicity with experimental allergic encephalomyelitis.

Cytotoxicity of immune lymph node cells in experimental allergic encephalomyelitis (EAE) was maximal 9 days after injection of encephalitogenic emulsion. The ability of these cells to passively transfer EAE was also maximal at this time. Immune spleen cells were more cytotoxic than lymph node cells 9 days after injection; however, these cells did not passively transfer EAE. Twelve days after injection of encephalitogenic emulsion immune spleen cells passively transferred EAE with resulting mild histopathologic lesions. At this time the spleen cells were 50% more cytotoxic than comparable lymph node cells. Cyclophosphamide suppressed the development of clinical EAE and the development of cytotoxic lymphoid cells. It also reduced clinical signs and cytotoxic activity of lymph node cells. Spleen cell cytotoxic activity was enhanced by Cyclophosphamide. It was concluded that cytotoxic activity of lymph node and spleen cells was correlated with the ability of these cells to produce EAE. Lymph node cell populations differed qualitatively and/or quantitatively from immune spleen cell populations in EAE. Capacity to passively transfer EAE coincided with the maximal Cytotoxicity of the lymphoid cells from each tissue.     

Lipid peroxidation in experimental allergic encephalomyelitis

Lipid peroxidation (LPO) in the brain and blood of guinea-pigs was studied during experimental allergic encephalomyelitis. The most pronounced activation of LPO in the brain occurred at the 7th day of sensitization with encephalolitogenic emulsion. It manifested by an increase in the content of diene conjugates and malonic dialdehyde, activation of catalase and reduction of superoxide dismutase activity. LPO activation in the blood occurred at the 3th-5th day of sensitization. It is assumed that LPO activation is caused by antigen-antibody reaction that occurs in the blood at the 3d day and in the brain at the 7th day of sensitization.     

Active induction of experimental allergic encephalomyelitis

This protocol details a method to actively induce experimental allergic encephalomyelitis (EAE), a widely used animal model for studies of multiple sclerosis. EAE is induced by stimulating T-cell-mediated immunity to myelin antigens. Active induction of EAE is accomplished by immunization with myelin antigens emulsified in adjuvant. This protocol focuses on induction of EAE in mice; however, the same principles apply to EAE induction in other species. EAE in rodents is manifested typically as ascending flaccid paralysis with inflammation targeting the spinal cord. However, more diverse clinical signs can occur in certain strain/antigen combinations in rodents and in other species, reflecting increased inflammation in the brain.     

Passive induction of experimental allergic encephalomyelitis

Experimental allergic encephalomyelitis (EAE) is a widely used animal model of the human demyelinating disease multiple sclerosis. EAE is initiated by immunization with myelin antigens in adjuvant or by adoptive transfer of myelin-specific T cells, resulting in inflammatory infiltrates and demyelination in the central nervous system. Induction of EAE in rodents typically results in ascending flaccid paralysis with inflammation primarily targeting the spinal cord. This protocol describes passive induction of EAE by adoptive transfer of T cells isolated from mice primed with myelin antigens into na?ve mice. The advantages of using this method versus active induction of EAE are discussed.     

Niridazole suppression of experimental allergic encephalomyelitis in Lewis rats.

Administration of niridazole to Lewis rats beginning 2 days before sensitization with guinea pig spinal cord in combination with immunologic adjuvants exerted a dose related suppressive influence on development of experimental allergic encephalomyelitis (EAE). A daily dose of 75 mg/kg completely prevented clinical neurologic signs as well as markedly suppressed occurrence of immunohistopathologic manifestations of this autoimmune disease. A higher daily dose level of niridazole, i.e., 100 mg/k, also inhibited EAE but was associated with neurotoxic manifestations.     

Suppressor cell control of unresponsiveness to experimental allergic encephalomyelitis.

Lymph node cells (LNC) from Lewis rats rendered unresponsive to experimental allergic encephalomyelitis (EAE) by pretreatment with myelin basic protein markedly suppressed clinical (but not histologic) EAE in normal recipients later challenged with an encephalitogenic emulsion. Unresponsiveness was immunologically specific, and required viable LNC; serum transfer was ineffective. These findings suggest that suppressor cells exert control over this autoimmune disease.     

Myelin metabolism in vitro in experimental allergic encephalomyelitis

Abstract— Spinal cord slices from rats in different stages of allergic encephalomyelitis (EAE) were incubated with [U-¹⁴C]glucose. Normal rats and rats injected with Freund's adjuvant served as controls. The slices were fractionated by a discontinuous sucrose gradient into purified myelin and a heavy membrane residue, the lipids and proteins were extracted, and their specific activities were determined. Uptake of ¹⁴C into myelin lipids was depressed in the rats with acute EAE, while an increase was shown in myelin protein and heavy membrane lipids and proteins. The increased synthesis in non-myelin fractions was ascribed to invasion of metabolically active cells. The depression in myelin lipid synthesis occurred early in the disease before lesions appeared or the inflammatory reaction became widespread. Myelin from guinea pigs with acute EAE resulting from injection of a purified basic protein also showed a depression of uptake in both lipids and proteins. It is suggested that a metabolic insult as a result of the immunological process is dealt the oligodendroglial cells early in the course of the disease which leads to a weakening of the myelin sheath and subsequent phagocytosis of myelin.