【摘要】 为探讨神经肽对银屑病免疫细胞的调节,及其在银屑病神经免疫发病机制中的作用,本研究利用体外细胞培养技术分离培养单核细胞,分别加入外源性神经肽降钙素基因相关肽(calcitoningene-relatedpeptide,CGRP)及其受体拮抗剂CGRP8-37。用ELISA检测培养单核细胞上清液中趋化因子的含量;利用微型趋化小室,观察CGRP对单核细胞趋化活性的调节。结果CGRP诱导银屑病活化的单核细胞分泌趋化因子巨噬细胞炎性蛋白-1α(macrophageinflammatoryprotein-1α,MIP-1α)和单核细胞趋化性蛋白-1α(monocytechemotacticprotein-1α,MCP-1α)增加,受体拮抗剂CGRP8-37则抑制这种诱导作用,同时CGRP促进单核细胞对淋巴细胞和中性粒细胞的趋化活性,用CGRP8-37后则趋化活性减弱。提示银屑病皮损内神经肽CGRP可以通过受体诱导单核巨噬细胞分泌MIP-1α和MCP-1α趋化因子,使淋巴细胞和中性粒细胞在局部皮损区定向迁移与聚集,促进局部炎性细胞的浸润。更多还原

【Abstract】 The study is to investigate the regulation of neuropeptide calcitonin gene related peptide(CGRP) in immune cells, and the effect of neuropeptides on the neuroimmunopathogenesis of psoriasis. The monocytes from psoriasis patients were cultured in vitro. CGRP and antagonist CGRP8 37 were added into the LPS stimulated monocytes respectively . ELISA was used to determine the chemokine level in the cultured cells. Micro chemotacxis chamber was used to determine the chemotactic activity of the monocytes to neutrophils and lymphocytes. CGRP induced increased secretion of chemokine MIP 1α and MCP 1α in LPS stimulated monocytes. CGRP enhanced the chemotactic activity of LPS stimulated monocytes to neutrophils and lymphocytes. The antagonist CGRP8 37 inhibited the effect of CGRP on the monocytes. It is suggested that the neuropeptide CGRP from psoriatic lesion is probably to be able to regulate the chemotactic function of cutaneous immuno cells via specific receptors and enhance local inflammatory process.更多还原