Encephalomyelitis, allergic/autoimmune experimental

Genetically predisposed animals or induced animal models may also be used to study and predict chemical-induced autoimmunity. In induced models, a susceptible animal strain is immunized with a mixture of an adjuvant and an autoantigen isolated from the target organ. Examples are adjuvant arthritis (AA), experimental allergic encephalomyelitis (EAE) and experimental uveitis in the Lewis strain rat. Examples of spontaneous models... 

The cytokine transporters are not static but respond to physiological and pathological events. The transport rates of IL-1 and TNF each shov diurnal variations (Pan et al., 2002 Banks et al., 1998b). The hansport rate of TNF is altered in animals with experimental allergic/autoimmune encephalomyelitis (EAE), spinal cord injury, or blunt trauma to the brain (Pan et al., 1996 Pan et al., 1997a Pan and Kastin, 2001b Pan et al., 2003b). 

The role of ac tivated microglia in neuronal survival during inflammatory conditions has been extensively studied in the models of experimental allergic/autoimmune encephalomyelitis (EAE) and in the animal model of Multiple Sclerosis (MS) (Antel and Owens, 1999 Becher etal., 2000 Biemacki etal., 2005 Jack et al., 2005). A rapid recruitment of blood-borne monocytes, an... 

Experimental allergic encephalomyelitis (EAE). Autoimmune demyelinating disease induced in genetically susceptible mice, rats, or marmosets by immunization with myelin proteins or peptides. Animal model for multiple sclerosis. 

Experimental allergic encephalomyelitis is an animal model of autoimmune demyelination 640... 

Weigle, W.O. (1980). Analysis of autoimmunity through experimental models of thyroiditis and allergic encephalomyelitis. Adv. Immunol. 30 159-275. 

In autoimmunity models, similar interactions occur. Thus, mice exposed to S. mansoni ova are protected from two different autoimmune diseases, type 1 diabetes [71] and experimental allergic encephalomyelitis [72, 73]. In these instances, a Th2 immune deviation might equally explain the amelioration of Thl pathology, and experimental testing of this possibility remains to be undertaken. 

Riskind PN, Massacesi L, Doolittle TH, Hauser SL (1991) The role of prolactin in autoimmune demyelination suppression of experimental allergic encephalomyelitis by bromocriptine. Ann Neurol, 29(5) 542-547. 

Figure 7. The effect of K252a on the therapeutics and macrophage activation in the experimental autoimmune allergic encephalomyelitis. (A) EAE was induced by a common protocol, neurological examinations were daily performed and the mean neurological score was measured. The control animal groups received either carrier or immunized without any other treatment. (B) Peritoneal macrophages collected from the animal groups as presented in figure 7A, were isolated in F12 medium, divided in samples of 10 cells/ml and incubated with EPS (bacterial lipopolysacharides, 10 ng/ml) for 18 hours at 37°C. Thereafter NO release in the culture medium was measured as described by Denis, 1991. (C) NR-8383 rat alveolar macrophages were incubated for 18 hours at 37°C (10 cells/ml) with 1 ng/ml EPS in the presence of 1 pM mentioned alkaloids. NO release to the culture medium was measured as previously described.

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