Abstract
The autoimmune disease multiple sclerosis (MS), with strong inflammation and neurodegeneration, affects motor and cognitive functions. S100B is increased in CSF, serum and post-mortem plaques of MS patients being correlated with demyelination and glial reactivity. We also showed that S100B neutralization has a beneficial outcome in an ex vivo demyelinating model. Here, we first addressed how targeting S100B with pentamidine could prevent MS-related pathogenesis in the ex vivo model. Pentamidine prevented not only demyelination and axonal impairment, but also the exacerbated production of inflammatory factors (TNF-α, IL-1β, HMGB1). Next, we used the in-vivo animal model of MS, the Experimental Autoimmune Encephalomyelitis (EAE), to evaluate if pentamidine could prevent/ameliorate MS disease course. EAE-induced animals when treated with pentamidine reach a lower disease clinical score and have a fast recovery. Our results indicate that S100B is involved in MS pathology and that its inhibition may be a new potential therapy to reduce damage and improve recovery.
Published Version
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