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Disease Model | Experimental Autoimmune Encephalomyelitis (EAE) Animal Model

Introduction:

The symptoms, pathological changes, and immunological characteristics of the experimental autoimmune encephalomyelitis (EAE) animal model closely resemble those of human multiple sclerosis (MS) and acute disseminated encephalomyelitis; accordingly, this model is regarded as an ideal animal model for these diseases.

 

 

Experimental allergic encephalomyelitis (EAE) is a T‑lymphocyte‑mediated autoimmune disease that occurs in susceptible animals, characterized primarily by perivascular mononuclear cell infiltration and demyelination of the white matter in the central nervous system (CNS).

Select animals

Due to the distinct genetic backgrounds of different animal species or even different strains within the same species, their T-cell clones in the immune system exhibit varying responses to self‑antigens. Therefore, experimental animals should be selected based on their susceptibility to the EAE model.

EAE can be induced in a variety of animal species, ranging from birds to mammals. Animal models that are susceptible to EAE include Lewis rats, DA rats, PL mice, SLJ mice, and guinea pigs, among others.

The EAE model in rats closely resembles the human clinical presentation in terms of clinical manifestations, pathology, immunological features, and biochemical changes; therefore, we commonly use either rats (Wistar rats, 200–220 g) or mice (female C57BL/6 mice, 6–8 weeks old) for establishing animal models.

 

Construction method

  They are mainly divided into active induction and passive induction methods.

1. Active Induction Method

(1) Prepare the antigen and mix it with an adjuvant to form an antigen emulsion.

(2) Rats were injected with an antigen emulsion at the plantar surface (footpad), while mice received a subcutaneous injection of the antigen emulsion on the dorsal side of the spine. A second injection of pertussis toxin was administered 48 hours later.

(3) The day of injection is designated as Day 0. Body weight and clinical neurological function scores (according to the Kono scoring system) are recorded daily until 30 days post‑immunization.

(4) Lymph node cells from diseased animals were isolated and co-cultured with MBP, followed by an antigen-specific T-cell proliferation assay. T lymphocyte isolation and CD‑marker phenotyping were also performed. 

(5) Histopathological and immunohistochemical analysis of animal brain and spinal cord tissues 

Following disease onset, FACS analysis of brain‑derived lymphocytes revealed PKH2‑GL–labeled cells, whereas PKH2‑GL–positive cells were rarely detected in liver and spleen tissues, indicating organ specificity. 

 

Histological analysis of the cervical spinal cord

Under light microscopy, extensive inflammatory cell infiltration was observed in the brain and spinal cord tissues of the rats, with inflammatory cells clustered around blood vessels, giving rise to a cuffing pattern. 

 

Model features:

Animals develop clinical signs 9 to 11 days after antigen injection; severe cases may result in death, while surviving animals begin to recover gradually approximately three weeks post‑inoculation.

Special note: The site of antigen injection can influence the final outcomes of the EAE model, including the latency period, incidence rate, mortality rate, and relapse rate. 

2. Passive transfer experiment: 

Construction method: EAE antigen-specific T cells are isolated and transferred into healthy animals of the same strain (as blank control animals), thereby inducing disease in the recipient animals. 

(1) Collect lymph nodes from affected animals for cell culture and perform CD analysis. 4 Cell screening. 

(2) To determine the specific antigen‑specific response of cells, PKH2‑GL‑labeled cells are used, 

(3) Inject cells into healthy animals, observe clinical signs after 10 days, and isolate mononuclear cells from the brain and spinal cord for phenotypic analysis. 

Model features: The animal model established in this study is an ideal platform for investigating the pathogenesis, treatment, and prevention of EAE. It exhibits high reproducibility but lacks widespread primary demyelination. 。

Reference:

[1] Methodology for Replicating Animal Models of Human Diseases / Edited by Zhou Guangxing et al. — Shanghai: Shanghai Scientific & Technological Literature Publishing House, January 2008.

[2]Hervé Perron, Hei-Lanne Dougier-Reynaud. Human endogenous retrovirus protein activates innate immunity and promotes experimental allergic encephalomyelitis in mice. PLoS One [J]. 2013 Dec 6;8(12):e80128.

[3] TAI Shurhong, LI Hong. Establishment of a murine experimental autoimmune encephalomyelitis model and investigation of its immunological mechanisms. IMMUNOLOGICAL JOURNAL [J], Vol. 24, No. 1, Jan. 2008.

[4] Wei Wei, Tang Yi, Wei Luyun. Study on the changes in neuroglobin expression in EAE rats [J]. Journal of Immunology, 2010, (12): 1056-.

[5] Lü Xueying, Zhang Fengyun, Wang Liqun, et al. Pathological study of experimental allergic encephalomyelitis [J]. Chinese Journal of Neuroimmunology and Neurology, 2000, 7(1):3. 

 

 

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