EAE model_Biocytogen Pharmaceuticals (Beijing) Co., Ltd.

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EAE model

Introduction of experimental autoimmune encephalomyelitis (EAE) model

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that leads to encephalitis and demyelination. MS is considered an autoimmune disease caused by autoreactive T cells with symptoms including muscle rigidity and paralysis, visual disturbance and blindness, sensory loss and ataxia, and is characterized by recurrent relapses. At present, there are many different animal models of MS, of which the experimental autoimmune encephalomyelitis (EAE) model is widely used in the study of multiple sclerosis due to its pathological characteristics of inflammation and demyelination similar to MS.

In rodents such as mice and rats, EAE models can be induced by immunization with spinal cord homogenates, purified myelin, myelin proteins (e.g., myelin basic protein MBP, protein lipoprotein PLP, and myelin oligodendrocyte glycoprotein MOG), or peptides of these proteins. This may be because myelin-specific T cells are activated in the periphery, cross the blood-brain barrier into the central nervous system and are reactivated, triggering a series of inflammatory responses, leading to demyelination and axonal cell apoptosis, ultimately leading to nerve injury and loss of function. Clinical symptoms are assessed using a standardized scoring system, which measures the degree of induction of the disease, with focal demyelination and inflammatory leukocyte infiltration seen in the stained sections of the pathological tissue.

The MOG-induced EAE disease model protocol described here was established in C57BL/6 mice and in B-hIL17A humanized mice developed by Biocytogen, andcan be used for pharmacodynamic evaluation of MS-related drugs.

Establishment of EAE mouse model

Experimental Animals：C57BL/6, 10-13 weeks old, female

Modeling reagent：MOG emulsion and PTX

Modeling method：Immunized with MOG emulsion and injected pertussis toxin intraperitoneally

C57BL/6 mice (female, 8-week-old, n=5) immunized with MOG (myelin oligodendrocyte glycoprotein) emulsion, which were given PTX (pertussis toxin) on the day of immunization and the following day, respectively.(A) Body weight change of animals in each group. (B) Clinical scores of animals in each group. Compared with the untreated group (G1-Vehicle), the MOG-treated group (G2) had tail weakness, lameness, hind limb paralysis and other symptoms, resulting in an increased clinical score. This demonstrates that EAE was successfully induced in C57BL/6 mice. Data are shown as mean ± SEM.

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Local inflammatory responses in the central nervous system (CNS) of EAE model mice. Spinal cords were taken on day 35 after MOG and PTX immunization, and tissue sections were stained with H&E (A, B) and detected by immunofluorescence (IF) (C, D) (green: MBP; blue: DAPI). inflammatory cell infiltration (DAPI+ cells) was significantly increased and myelin protein was significantly reduced in the model group. This suggests that the EAE disease model was successfully induced in C57BL/6 mice.

Product list

Product name	Product number
B-hIL17A mice	110053
B-hTNFA mice	110002

References

1. Gaffen, S.L., Jain, R., Garg, A.V. & Cua, D.J. The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing. Nat Rev Immunol 14, 585-600 (2014).

2. Iwakura, Y. & Ishigame, H. The IL-23/IL-17 axis in inflammation. J Clin Invest 116, 1218-1222 (2006).

3. Kuwabara, T., Ishikawa, F., Kondo, M. & Kakiuchi, T. The Role of IL-17 and Related Cytokines in Inflammatory Autoimmune Diseases. Mediators Inflamm 2017, 3908061 (2017).