Is multiple sclerosis a proresolution deficiency disorder?

The inflammatory process seen in multiple sclerosis is due to an excess production of proinflammatory cytokines interleukin-1 (IL-1), IL-6, tumor necrosis factor-α, interferons, macrophage migration inhibitory factor, HMGB1 (high mobility group B1), and, possibly, a reduction in antiinflammatory cytokines IL-10, IL-4, and transforming growth factor-β that leads to increased secretion of reactive oxygen species, including nitric oxide, resulting in neuronal damage. It is suggested that failure of production of adequate amounts of resolution-inducing molecules lipoxins, resolvins, and protectins that suppress inflammation and reactive oxygen species production, enhance wound healing, and have neuroprotective properties results in inappropriate inflammation and delay in the healing/repair process, and so neuronal damage continues, as seen in multiple sclerosis. Hence, methods designed to enhance the production and/or administration of lipoxins, resolvins, and protectins may form a new approach in the prevention and treatment of multiple sclerosis and other similar autoimmune diseases.