title: Is multiple sclerosis a proresolution deficiency disorder?
abstract: 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.
authors.affiliation: UND Life Sciences, Shaker Heights, Ohio, USA. Undurti@hotmail.com
authors.forename: Undurti N
authors.initials: UN
authors.lastname: Das
mesh_terms: D003677:Deficiency Diseases / Q000150:complications* / Q000378:metabolism; D004281:Docosahexaenoic Acids / Q000172:deficiency* / Q000378:metabolism / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D018836:Inflammation Mediators / Q000378:metabolism; D044045:Lipoxins / Q000172:deficiency* / Q000378:metabolism / Q000627:therapeutic use; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D044045:Lipoxins; D017382:Reactive Oxygen Species; D004281:Docosahexaenoic Acids