Experimental autoimmune encephalomyelitis
Experimental autoimmune encephalomyelitis, sometimes Experimental Allergic Encephalomyelitis (EAE) is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases, including the diseases multiple sclerosis and acute disseminated encephalomyelitis (ADEM).
EAE was motivated by observations during the convalescence from viral diseases by Thomas M. Rivers, D. H. Sprunt and G. P. Berry in 1933. Their findings upon a transfer of inflamed patient tissue to primates was published in the Journal of Experimental Medicine article (Vol. 58, No. 1, pp. 39-56)[1][2]. An acute monophasic illness, it has been suggested that EAE is far more similar to ADEM than MS[3].
EAE can be induced by inoculation with whole CNS tissue, purified myelin basic protein (MBP) or myelin proteolipid protein (PLP), together with adjuvants. It may also be induced by the passive transfer of T cells specifically reactive to these myelin antigens. EAE may have either an acute or a chronic relapsing course. Acute EAE closely resembles the human disease acute disseminated encephalomyelitis, while chronic relapsing EAE resembles multiple sclerosis. EAE is also the prototype for T-cell-mediated autoimmune disease in general.
A video titled "Chronic relapsing-remitting experimental autoimmune encephalomyelitis (CR-EAE) in Dark Agouti rats" can be seen at http://www.veomed.com/va02173932009. A video titled "reatment of chronic relapsing-remitting EAE in rats with ShK-186, an inhibitor of Kv1.3 channels in effector memory T cells" can be seen at http://www.veomed.com/va0217262009.
EAE in mice
Demyelination is produced by injection of brain extracts (like myelin basic protein). The Blood-brain barrier is opened by injection of Freund adjuvant (adjuvant serves as BBB breaker).
Immune system of the animal ‘goes wild’ and multiple small disseminated lesions of demyelination (as well as micro-necroses) appear simultaneously in the brain.
Sharing some features, mostly demyelination, this model, first introduced in 1930s, cannot be considered equivalent to human MS. EAE either kills animals or leaves them with permanent disabilities, animals with EAE also suffer severe nerve inflammation, and the time course of EAE is entirely different from MS, being the main antigen (MBP) in charge.
References
- ^ Rivers TM, Spunt DH & Berry GP (1933). OBSERVATIONS ON ATTEMPTS TO PRODUCE ACUTE DISSEMINATED ENCEPHALOMYELITIS IN MONKEYS. Journal of Experimental Medicine 58:39-53.
- ^ Rivers TM & Schwentker FF. (1935). Encephalomyelitis accompanied by myelin destruction experimentally produced in monkeys. Journal of Experimental Medicine 61:689 –701.
- ^ Sriram S & Steiner I (2005) Experimental Allergic Encephalomyelitis: A misleading model of Multiple Sclerosis. Annals of Neurology 58:939 –945.
External links
- mult-sclerosis.org - Information on EAE
- More than 100, freely available, published research articles on EAE and related topics such as multiple sclerosis by Professor Michael P. Pender, Neuroimmunology Research Unit, The University of Queensland
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