Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) that mainly affects young adults, featuring gradual degeneration and loss of previously established functional myelin sheaths and, eventually, of oligodendrocytes. Data from animal model of MS, Experimental autoimmune encephalomyelitis (EAE), induced by immunization of susceptible mouse strains with different myelin components, provide a useful animal model for human multiple sclerosis. Myelin oligodendrocyte glycoprotein (MOG) is a transmembrane glycoprotein expressed on the surface of central nervous system (CNS) myelin membranes. Herein, we have used MOG35-55 peptide to induce EAE in mice. Following anesthesia (ketamin 40mg/kg + xylazin 4mg/kg), C57/BL6 mice have received bilaterally 150µg MOG35-55 emulsified in CFA containing 4mg/mL MT H37Ra. The cocktail was micro-surgically implanted at the base of the tail while the animals were lying on each side. A total amount of 200ng pertussis toxin (2.5 ng/ul in PBS) was given i.p. on days 0 and 2 p.i. The same volume of PBS was injected into a parallel group of mice as control. Clinical assessment of EAE was performed daily by scoring each of the following factors: flaccid tail; left and right hind limb weakness, abnormal gait or complete hind limb paralysis; left and right forelimb weakness or paralysis, moribund or deceased (0-3 graduations with 0.5 for intermediate scores). The results have revealed that MOG35-55 implanted mice have started showing the clinical abnormalities on day 7, reaching the maximum score of (9.81 ± 0.91) on day 18, followed by gradual decline of the scores. The control mice have shown no abnormalities (scored 0) among the whole experiment. This provides a practical method of inducing EAE and the resultant scoring protocol, which can be of benefit in the studies focused on human MS and its possible treatments.

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