| Guillain–Barre′Syndrome (GBS) is an acute immune-mediated perioheral nervous system diseases. It has been distributed all over the world, it has a high morbidity in our country. Experimental autoimmune neuritis (EAN) is a T- cell-mediated, inflammatory demyelinating disease of peripheral nervous system(PNS) that serves as a model for GBS in humans. It has histopathological, electrophysiological and clinical similarities to the GBS and therefore is used as an animal model to understand the pathogenesis of GBS.In recent years there have been a number of studies examining the kinetics and function of cytokines, and other growth factors during the course of myelin induced EAN in the Lewis rat. Many observations show that neutralization of TNF with sTNFR I can inhibit the development of EAN and confirm that TNF plays a prominent role in autoimmune diseases. The principal ameliorative effects of sTNFR I therapy would be to neutralize TNF activity, thereby reducing TNF mediated pathology. Depression of T-cell proliferation and IFN-γsecretion, as well as decreased local lymphocytic traffic resulting from sTNFR I neutralization of TNF, probably play an essential role in this protection. In our study, we investigated the effects of soluble TNFR type I (sTNFR I) in EAN induced in mice by P0 peptide 180–199 and Freund's complete adjuvant. Our data from two different therapeutic regimens indicate that the administration of sTNFR I effectively ameliorated the clinical and pathological signs of EAN, i.e., decreased its severity, shortened its duration, and reduced inflammatory cell infiltration into the peripheral nervous system. These data emphasize a central role of TNF during the process of EAN and also indicate beneficial effects of soluble TNF receptors in the treatment of EAN. These data directly demonstrate a pivotal role for TNF in the development of EAN and also suggest that sTNFR I may have therapeutic potential for alleviating GBS in humans.Objective:1. To study probability of in experimental autoimmune neuritis with P0 180-199 peptide induced and provide a good and available animal models for basic researches of GBS.2. To elucidate the effect of sTNFR I on EAN by it's symptoms and macrophages, or CD4 + or CD8 + T cells.3. To elucidate the effect of sTNFR I on EAN by it's secretion of TNF-αand production of IL-4Methods:EAN animal model was established by immunizing female Lewis rats (6-8 weeks) with P0 180-199 peptide and completed Freund's adjuvant ( CFA ). A total of 30 healthy adult female Lewis rats were randomly divided into control group, sTNFR I treated group and PBS (phosphate buffered saline) treated group. EAN model Lewis were determined by measurement clinical score and Infiltration of lymphocytes and macrophages in sciatic nerves sections and demyelination in sciatic nerves of Lewis rats The animals were given sTNFR I or PBS intraperitoneally. Then histopathological and immunological methods were used after treatment , respectively, to detect the effect of sTNFR I on EAN.Results:Signs of EAN occurred in 77% of Lewis rats in the EAN group ,which was confirmed by the clinical score>1.5 grade and the demyelination in sciatic nerves of Lewis rats. Compared with PBS treated group, sTNFR I treated group displayed less severe clinical sign, decreased infiltration of inflammatory cells into sciatic nerves,milder demyelination, decreased infiltration of macrophages, or CD4 + or CD8 + T cells into sciatic nerves , reduced secretion of TNF-αand increased production of IL-4 .Conclusions:1. Immunization with the P0 180-199 peptide can induce EAN in Lewis rats .The achievement ratio of EAN model was 77% . This animal models builds a base for basic researches of GBS.2.sTNFR I plays an important role in amelioration of EAN.
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