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Delayed, relapsing experimental allergic encephalomyelitis in mice

F D Lublin, P H Maurer, R G Berry

    Journal of Immunology (Baltimore, Md. : 1950)
    |March 1, 1981
    PubMed
    Summary
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    This study developed a mouse model of relapsing experimental allergic encephalomyelitis (EAE) that mimics multiple sclerosis. The delayed-onset, relapsing-remitting disease shows both acute and chronic central nervous system lesions.

    Area of Science:

    • Neuroimmunology
    • Demyelinating diseases
    • Animal models of neurological disorders

    Background:

    • Experimental allergic encephalomyelitis (EAE) is a common animal model for studying demyelinating diseases.
    • Existing EAE models often present as acute, monophasic disease, which does not fully recapitulate the complexity of human neurological conditions like multiple sclerosis.
    • There is a need for EAE models that exhibit a relapsing-remitting disease course and pathology reflective of chronic and active lesions.

    Purpose of the Study:

    • To establish and characterize a novel mouse model of experimental allergic encephalomyelitis (EAE) with a delayed onset and relapsing-remitting clinical course.
    • To evaluate the pathological features of this model, focusing on demyelination and inflammation in the central nervous system.
    • To determine if this model more closely resembles the pathology and clinical presentation of multiple sclerosis (MS) compared to acute EAE models.

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    Main Methods:

    • Female SJL mice were immunized with an emulsion containing lyophilized mouse spinal cord, pertussis vaccine, and complete Freund's adjuvant.
    • Clinical signs of EAE were monitored for disease onset, relapses, and severity over an extended period.
    • Post-mortem pathological examination of the brain and spinal cord was performed to assess inflammatory infiltrates and demyelination.

    Main Results:

    • Immunization induced a delayed form of EAE (DR-EAE) with initial disease signs appearing around 6 months post-immunization.
    • The model exhibited a relapsing-remitting clinical course, with relapses occurring between 2 weeks and 11 months after the initial illness, and some mice experienced multiple relapses.
    • Pathological findings included perivascular mononuclear cell infiltration, acute demyelination, and the presence of subacute and chronic demyelinating lesions ('plaques') in the central nervous system.

    Conclusions:

    • The developed DR-EAE model in SJL mice effectively replicates a relapsing-remitting disease course.
    • The observed pathology, featuring both recent and old inflammatory lesions, closely mirrors the characteristics of multiple sclerosis.
    • This model serves as a valuable tool for investigating the pathogenesis and potential therapeutics for relapsing forms of demyelinating diseases, particularly multiple sclerosis.