More than half of people with multiple sclerosis experience severe quality of life impairment as a result of chronic pain. Experimental autoimmune encephalomyelitis is a model of multiple sclerosis that typically presents with paralysis of the hind limb, neuro inflammation, and neuro degeneration. Despite the absence of apparent hypersensitivity observed post-peak disease, this paralysis may prevent the use of pain behavior tests. We sought to optimize the pain phenotype of the traditional actively-induced EAE model. MOG35-55/CFA and 100–600ng pertussis toxin were used to induce EAE, and mechanical, cold, and thermal sensitivity was measured in the mice after 28 days. In order to evaluate demyelination and neuro inflammation, spinal cord tissue was collected 14 and 28 days after the injection. Mechanical hypersensitivity was only seen in mice that received 100ng of PTX. Demyelination, immune cell recruitment, cytokine expression, glial activation, and neuronal damage are hallmarks of disease pathology. EAE mice induced with moderate (200ng) doses of pertussis toxin outperformed EAE mice treated with low levels (100ng).In both EAE groups, immune staining revealed activated astrocytes and myeloid/microglial cells. Based on these findings, it may be possible to study pain behaviors in patients with EAE who still exhibit disease pathology. The mechanisms underlying pain may be better studied with this altered model. Over 2.5 million people worldwide suffer from Multiple Sclerosis (MS); an autoimmune disease of the nervous system.MS is thought to be started by a CD4+T cell-mediated response that attacks the myelin sheaths that surround axons. This causes significant motor, sensory, and cognitive deficits, as well as autonomic dysfunction, fatigue, and pain. The exact cause of MS is unknown. A common murine model of multiple sclerosis that mimics many of these symptoms is experimental autoimmune encephalomyelitis, which can be induced by adoptive transfer of encephalitogenic T cells into naive animals or by administering myelin protein/peptides as an adjuvant. The onset of clinical symptoms one to two weeks after disease onset serves as a useful model for investigating potential mechanisms underlying disease outcomes. Neuro inflammation, demyelination of the brain and spinal cord, as well as changes in functional outcomes like motor function loss and altered sensory outcomes are hallmarks of EAE, which is similar to MS. Pain is a symptom that is very common in multiple sclerosis and has a positive correlation with disability and poor quality of life related to MS. MS pain can sometimes be lesional or secondary. However, the underlying causes of MS's chronic neuropathic pain are largely unknown. To investigate the pathophysiology of central neuropathic pain in MS, it is essential to employ a trustworthy animal model, such as those developed by other groups. Like individuals living with MS, enlistment of EAE in the mouse brings about the presence of cold and mechanical allodynia before the beginning of engine shortfalls; intriguingly, neither EAE animals nor MS sufferers typically exhibit thermal hyperalgesia, which is hypersensitivity to noxious stimuli like intense heat. However, there is a gap between MS and EAE pain: While most people with MS experience an increase in pain sensitivity as their disease and symptoms progress, EAE animals exhibit a diminished or absent response to sensory stimuli during the diseases peak and chronic phases.

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Regards,
Catherine
Journal Co-Ordinator
Journal of Clinical Immunology and Allergy