Peripheral viral challenge exacerbates experimental autoimmune encephalomyelitis
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Peripheral viral infections are potent triggers of exacerbation in multiple sclerosis (MS). Here, we used a preclinical model of MS, the experimental autoimmune encephalomyelitis (EAE) to corroborate this comorbidity in an experimental setting. EAE was induced by immunization of mice with MOG peptide, and paralysis was scored using a 5-point scale. At the onset of the chronic phase of the disease (Days 42–58 after MOG injection) the animals were divided into low responders (LR) and high responders (HR) with the mean score of 1.5 and 2.5, respectively. The acute phase response (APR) was induced by intraperitoneal injections of a viral mimetic, polyinosinic-polycytidylic acid (PIC). Two daily injections were performed on Days 42 and 44 (PIC42,44 challenge) and on Days 54, 55 and 56 (PIC54,55,56 challenge). PIC42,44 challenge had no effect of EAE disease, whereas PIC54,55,56 challenge rapidly increased paralysis but only in HR group. This exacerbation ultimately led to animal death by Day 58. These results demonstrate that antiviral APR is a potent exacerbator of EAE, and that this activity directly correlates with the severity of the disease. This in turn, indicates that antiviral APR might play a pivot role in linking peripheral viral infections with MS exacerbations.
KeywordsPolyinosinic-polycytidylic acid Experimental autoimmune encephalomyelitis Inflammatory mediators Viral challenge Acute phase response Multiple sclerosis
This study was supported by a Pilot Grant from the National Multiple Sclerosis Society awarded to G.W.K.
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Conflict of interest
The authors declare no conflicts of interest.
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