Experimental autoimmune encephalomyelitis

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The experimental autoimmune encephalomyelitis (EAE), formerly referred to as experimental allergic encephalomyelitis referred to is one with the human multiple sclerosis comparable (MS) inflammatory disease of the central nervous system (CNS) in laboratory animals , which by the injection of various proteins is triggered.

The EAE is used in experimental biomedical research as an animal model for MS, in particular when studying the pathogenesis and testing new therapeutic approaches. The proteins used to trigger an EAE, such as myelin basic protein (MBP), proteolipid protein (PLP) or myelin oligodendrocyte glycoprotein (MOG), are part of the myelin present in the CNS . The injection causes an autoimmune process that is similar to multiple sclerosis both in terms of a number of important symptoms and in terms of the pathological basis. As with MS, EAE also leads to inflammation, destruction of the myelin sheath around the axons of the nerve cells known as demyelination , and loss of nerve cells and nerve fibers.

In contrast to MS, demyelination is less pronounced in EAE. In addition, inflammatory foci are more common in EAE than in MS in the spinal cord . In contrast to MS, which is usually characterized by a chronic and relapsing or phase-wise course with repeated regression of the symptoms, EAE occurs acutely and monophasic with permanent neurological deficits. In this respect, EAE is more similar to the rarely occurring acute disseminated encephalomyelitis (ADEM) or a specific stage of MS. The laboratory animals most commonly used for research on EAE are mice , but the disease can also be induced in rats , guinea pigs , rabbits, and primates .

The EAE model goes back to the work of the American virologist Thomas Milton Rivers in the mid-1930s on the question of why vaccination against rabies at that time rarely led to paralysis . His investigations into the injection of brain extracts from rabbits into rhesus monkeys , which are considered to be the origin of the EAE model, were continued in the mid-1940s by the American immunologist Elvin A. Kabat through the use of Freund's adjuvant . Since the induction of EAE without adjuvant would be very time-consuming or not possible depending on the species, the use of adjuvant has been standard in the currently used EAE models since then. In individual animal species or test animal strains, however, EAE can also be produced efficiently and reproducibly without an adjuvant.

literature

  • Eilhard Mix, Hans Meyer-Rienecker, Hans-Peter Hartung, Uwe K. Zettl: Animal Models of Multiple Sclerosis - Potentials and Limitations. In: Progress in Neurobiology. 92 (3) / 2010. Elsevier, pp. 386-404, ISSN  0301-0082
  • Andrew L. Croxford, Florian C. Kurschus, Ari Waisman: Mouse Models for Multiple Sclerosis: Historical Facts and Future Implications. In: Biochimica et Biophysica Acta - Molecular Basis of Disease. 1812 (2 )/2011. Elsevier, pp. 177-183, ISSN  0925-4439

Individual evidence

  1. ^ TM Rivers, FF Schwentker: Encephalomyelitis accompanied by myelin destruction experimentally produced in monkeys. In: Journal of Experimental Medicine. 61 (5) / 1935, pp. 689-702
  2. ^ HL Van Epps: Thomas Rivers and the EAE model. In: Journal of Experimental Medicine. 202 (1) / 2005, p. 4
  3. ^ E. Kabat, A. Wolf, AE Bezer: The rapid production of acute disseminated encephalomyelitis in rhesus monkeys by injection of heterologous and homologous brain tissue with adjuvants. In: Journal of Experimental Medicine. 85 (1) / 1947, pp. 117-130
  4. ↑ S. Stosic-Grujicic, Z. Ramic, V. Bumbasirevic L. Harhaji, M. Mostarica-Stojkovic: Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant. In: Clinical and Experimental Immunology. 136 (1) / 2004, 49-55

Web links

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