摘要
目的 研究多发性硬化 ( MS)患者趋化因子单核细胞趋化蛋白 ( MCP-1 ) m RNA在实验性自身免疫性脑脊髓炎 ( EAE)中的表达 ;经鼻黏膜给予 IFN-β1 b对 EAE趋化因子表达的影响。方法 运用同种鼠脊髓匀浆诱导EAE动物模型 ,主动免疫动物后通过鼻黏膜给 IFN-β1 b或 PBS连续 7d,于免疫后 8、1 2、1 8d用免疫组化法、原位杂交法检测其脑、脊髓组织及脾脏中 MCP-1的表达。结果 主动免疫 1 2 d,EAE进入症状高峰期 ,脑和脊髓组织以及脾淋巴细胞中 MCP-1高表达 ,与 8及 1 2 d组相比差异有显著性 ,IFN-β 1 b组 MCP-1表达受到明显抑制 ,以 1 2 d组最为明显 ,与 EAE组相比差异有显著性。结论 MCP-1与 EAE的发病密切相关 ,外周表达早于组织 ,鼻服 IFN-β1 b可抑制外周淋巴细胞 MCP-1表达 ,减少中枢神经系统内炎性细胞浸润 ,使 EAE发病明显减轻。
Objective To employ the animal model EAE to examine the monocyte chemoatactic protein(MCP-1) mRNA expression in EAE and the effects of IFN-β 1b. Methods EAE was induced in Tun rats with rat spinal cord homogenate in complete Freund adjuvant (CFA). The rats were scored for the development of clinical EAE. The expression of MCP-1 mRNA was examined at the preclinical peak, and recovery stages in situ hybridization. EAE rats were treated with total dosage(3.5 μg) of IFN-β 1b or PBS on seven consecutive days after immunazation and tested for the suppression of MCP-1 mRNA. The control group received normal saline at the same dose.Results The expression of MCP-1 mRNA was upregulated concurrently with symptom onset of EAE and correlated with the intensity of inflammatory changes. The highest expression was detected at the peak of the disease. Treatment of IFN-β 1b significantly suppressed the expression of MCP-1 mRNA.Conclusions MCP-1 plays a role in the immunopathogenesis of EAE, and that MCP-1 induced trafficking of inflammatory cells can be inhibited by IFN-β 1b in the peripheral first and then the CNS. Further elucidation of the regulation and coordination of MCP-1 may lead to a new therapeutic approach to MS in humans.
出处
《中国神经免疫学和神经病学杂志》
CAS
2003年第3期166-170,共5页
Chinese Journal of Neuroimmunology and Neurology
基金
湖南省自然科学基金资助项目 ( 0 0 1jjy2 0 80 )
关键词
实验性自身免疫性脑脊髓炎
趋化因子
细胞免疫
原位杂交
experimental autimmune encephalomyelitis
cellular immunization
chemokine
in situ hybridization
