Eicosenoids Modify Experimental Allergic Encephalomyelitis.

摘要: Experimental allergic encephalomyelitis (EAE) is an autoimmune inflammatory disease of the brain and spinal cord. It animal model postinfectious multiple sclerosis (MS). In EAE in MS, monocytes Th1 lymphocytes penetrate blood-brain barrier, ensuing inflammation causes demyelination death oligodendroglia. PGE a product blood Mo glial cells that affects immune regulation. other cAMP agonists inhibit monocyte function secretion cytokines by cells. However, they have minimal effects on some secreted Th2 We hypothesized eicosenoids would central nervous system mediated found misoprostol, long-acting PGE1 analog, inhibited clinical histological signs moderately severe Lewis rats. Indomethacin also suppressed enhanced LAPGE effect. Both agents when administered either from time immunization or onset disease. The combination misoprostol indomethacin delayed-type hypersensitivity reactions to MBP (a response). These vitro lymphocyte proliferation mitogens MBP. Leukotrienes (LKT) elevate intracellular cGMP amplify responses, opposite agonists. LKT synthesis inhibitors blocked EAE, presumably lowering levels Reduction plus EAE. analogs, indomethacin, block responses antigens vivo. Modification with these may ameliorate diseases.