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Investigating mechanisms underlying the development of paralysis symptom in a model of MS
Shruti Gupta1, Sreejita Arnab1, Noah Silver-Beck2
1Department of Anatomy and Cell Biology, The George Washington University, Ross Hall, Washington D.C. 20052, United States.
Abstract:
Multiple sclerosis (MS) is an autoimmune neurodegenerative disorder with approximately 80 % of patients suffering from pain and 50 % from paralysis. Using a rodent model for MS, experimental autoimmune encephalomyelitis (EAE), researchers have predominately investigated paralysis/motor disease as the clinical symptom of EAE with fewer studying MS/EAE pain. However, in EAE, all mice exhibit a pain like phenotype and only a subset progresses to paralysis. Despite extensive research characterizing the disease pathology, the etiology that contributes to the range of pain and motor symptom occurrence in MS remains understudied. This is the first study to dissect MS symptom pathophysiology, using the non-PTX EAE model, in mice that experience mechanical hypersensitivity (pain-like phenotype) with and without paralysis. We found that mechanical hypersensitivity experienced by mice with or without paralysis is comparable between the two groups, irrespective of sex. In addition, there is a significant increase in the activation and infiltration of immune cells, demyelination, and heightened protein expression of B cell chemoattractant CXCL13 within the spinal cord of mice exhibiting mechanical hypersensitivity and paralysis, compared to mice only experiencing mechanical hypersensitivity.
Insights
Multiple sclerosis (MS) pain is comparable in mice with or without paralysis. However, paralysis involves increased immune cell activation, demyelination, and CXCL13 in the spinal cord.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Multiple sclerosis (MS) is a neurodegenerative autoimmune disorder impacting many patients with pain and paralysis.
- Research has focused on paralysis in experimental autoimmune encephalomyelitis (EAE), a rodent model for MS, with less attention to MS-associated pain.
- The underlying causes for the varying severity of pain and motor symptoms in MS remain understudied.
Purpose of the Study:
- This study aimed to dissect the pathophysiology of MS symptoms in a non-PTX EAE model.
- The research compared mice experiencing mechanical hypersensitivity (pain) with and without paralysis.
Main Methods:
- Utilized the non-PTX EAE rodent model to study MS pathophysiology.
- Assessed mechanical hypersensitivity, paralysis, immune cell activation and infiltration, demyelination, and CXCL13 protein expression in the spinal cord.
Main Results:
- Mechanical hypersensitivity was comparable between EAE mice with and without paralysis, irrespective of sex.
- Mice with both mechanical hypersensitivity and paralysis showed significantly increased immune cell activation and infiltration, demyelination, and CXCL13 protein levels in the spinal cord compared to those with only hypersensitivity.
Conclusions:
- Pain-like phenotypes in EAE are not solely dependent on the presence of paralysis.
- Paralysis in EAE is associated with distinct pathological changes in the spinal cord, including heightened neuroinflammation and demyelination, potentially mediated by CXCL13.
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