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趋化因子mRNA在实验性变态反应性神经炎中表达的研究 被引量:1

C-C Chemokine mRNA expression in murin experimental allergic neuritis
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摘要 目的:实验性变态反应性神经炎(EAN)是一类T细胞介导的周围神经系统的自身免疫病,可用牛坐骨神经加完全氟氏佐剂诱导而成。本文研究趋化因子mRNA在实验性变态反应性神经炎(EAN)中的表达并探索其可能的作用。方法:用兔坐骨神经匀浆免疫Wistar大鼠,诱导格林巴利综合症(GBS)的动物模型EAN;采用地高辛标记的寡核苷酸探针检测EAN病变神经组织浸润细胞上趋化因子单核细胞趋化蛋白-1(MCP-1)及巨噬细胞炎性蛋白-1β(MIP-1β)mRNA表达情况。结果:MCP-1mRNA在临床症状出现前1-2天(14天)水平最高,随后逐渐下降;MIP-1 βmRA在临床症状出现前1-2天水平开始升高,在临床症状达到高峰时(21天)最高,进入恢复期后降至基础水平。结论:趋化因子在EAN的炎性细胞迁移及浸润进入神经细胞过程中起到重要作用。 Objective: Experimental autoimmune neuricis (EAN) is a T-cell-mediated autoimmune disease of the peripheral nervous system (PNS) that can be actively induced in Lewis rats by imunization with bovine PNS myelin and Freund's complete adjuvant. In the present study, the dynamics of the expression of C-C chemokines mRNA of macrophage inflanr matory protein-1 β(MIP-1β) and monocyte chemotactic protein-1(MCP-1) were determined in the sciatic nerves of EAN. Methods: The mRNA of MIP-1β and MCP-1 were identified in infiltrating cells in sciatic nerve sections over the course of EAN by in situ hybridization (ISH) using digoxingenin labeled riboprobes. Results: The maximum of mRNA encoding MIP-1β positive cells in the scitic nerves was seen en day 21 post immunization (p. i. ) correlating with the development of severe clinical signs. Peak numbers of MCP-1 mRNA positive cellswere induced in the infiltrating cells in sciatic nerves l-2days before clinical signs were apparent of EAN, favoring a role for these chemokines in disease development. Conclusion: These results define a subset of chemokines that may play an important role in the inflammatory process during muring EAN and have relevance for future studies on pathogenesis and treatment of GBS in humans.
出处 《脑与神经疾病杂志》 2000年第5期257-261,共5页 Journal of Brain and Nervous Diseases
关键词 趋化因子 实验性变态反应性神经炎 炎性反应 Chemokine Experimental autoimmune neuritis Inflammation.
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  • 1Hedrick J A, Saylor V, Figueroa D, et al, Lymphotactin is produced by NK cells and attracts both NK cells and T cells in vivo [J]. J Immunol, 1997, 158 (4):1533-1540.
  • 2Pan Y, Lloyd C, Zhou H, et al. Neurotactin, a membrane-anchored chemokine upregulated in brain inflammation[J]. Nature,1997,387(6633) :611-617.
  • 3Fujioka T, Purev E, Rostami A, et al. Chemokine mRNA expression in the cauda of lewis rats with experimental allergic neuritis[J]. J Neuroimmunol, 1999,97(1-2) :51-59.
  • 4Orlikowski D, Chazaud B, Plonquet A, et al. Monocyte chemoattraetant protein-1 and chemokine receptor CCR2 production in Guillain-Barre sydrome and experimental autoimmune neuritis [J]. J Neuroimmunol,2003,134(1-2):118-127.
  • 5Kieseier BC, Krivacic K, Jung S, et al. Sequential expression of chemokines in experimental autoimmue neuritis[J]. J Neuroimmunol, 2000, 110 ( 1-2 ) : 121-129.
  • 6Zou LP, Pelidou SH, Abbas N, et al. Dynamics of production of MIP-lalpha, MCP-1 and MCP-2 and potential role of neutralization of these chemokines in the regulation of immune responses during experimental autoimmune neuritis in Lewis rats[J]. J Neuroimmunol,1999,98(2):168-175.
  • 7Kieseier BC, Tani M, Mahad D, et al. Chemokines and chemokine receptors inflammatory demyelinating neuropathies:a central role for IP-10[J]. Brain,2002, 125(4) :823-834.
  • 8Mahad DJ,Howell SJL, Woodroofe MN, et al. Expression of chemokines in cerebrospinal fluid and serum of patients with chronic inflammatory demyelianting polyneuropathy[J]. J Neuro Neurosurg Psychia, 2002,73:320-323.
  • 9Muller-Ladner U, Jones JL, Wetsel RA, et al. Enhanced expression of chemotactic receptors in multiple sclerosis lesion[J]. J Neurolsci, 1996, 144 (1-2):135-141.
  • 10Zou LP, Ma DH,Wei L,et al. IFN-beta suppresses experimental autoimmune neuritis in Lewis rats by inhibiting the migration of inflammatory cells into peripheral nervous tissue[J]. J Neurosci Res, 1999,56(2): 123-130.

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