MIP⁃3α和CCR6参与调控空肠Ⅰ型闭锁隔膜组织免疫应答的组织学研究  

Expressions of macrophage inflammatory protein⁃3αand chemokine receptor 6 in septum derived from type I intestinal atresia

作　　者：刘雪来[1] 叶茂 谢向辉 李龙[1] 宋岩彪 李索林[3] 高鹏 崔钊[5] Liu Xuelai;Ye Mao;Xie Xianghui;Li Long;Song Yanbiao;Li Suolin;Gao Peng;Cui Zhao(Department of Surgery,Capital Institute of Pediatrics&Affiliated Children's Hospital,Beijing 100020,China;Department of Central Laboratory,Second Hospital,Hebei Medical University,Shijiazhuang 050000,China;Department of Pediatric Surgery,Second Hospital,Hebei Medical University,Shijiazhuang 050000,China;Department of Surgery,Harbin Children's Hospital,Harbin 150010,China;Department of Surgery,Changchun Children's Hospital,Changchun 130061,China)

机构地区：[1]首都儿科研究所附属儿童医院外科,北京100020 [2]河北医科大学第二医院中心实验室,石家庄050000 [3]河北医科大学第二医院小儿外科,石家庄050000 [4]哈尔滨市儿童医院外科,哈尔滨150010 [5]长春市儿童医院外科,长春130061

出　　处：《中华小儿外科杂志》2022年第11期1044-1048,共5页Chinese Journal of Pediatric Surgery

基　　金：北京市自然科学基金项目(7222015);北京市属医学科研院所公益发展改革试点项目(京医研2019⁃11)。

摘　　要：目的观察和比较先天性空肠Ⅰ型闭锁隔膜组织黏膜层内趋化因子受体6(chemokine receptor,CCR6)和巨噬细胞炎性蛋白⁃3α(macrophage inflammatory protein⁃3α,MIP⁃3α)的表达。方法选用距离Treitz韧带15 cm以内的空肠Ⅰ型闭锁患儿的隔膜组织为研究组(12例),以同一患儿术中行肠切除肠吻合过程中钳取收集的正常肠壁组织为对照组(12例)。采用免疫组织化学染色法进行半定量比较两组CCR6和MIP⁃3α的表达差异。结果免疫组织化学染色结果显示正常肠壁组织黏膜层内未见CCR6表达,隔膜组织黏膜层可见CCR6表达。正常肠壁组织和隔膜组织黏膜层均可见MIP⁃3α表达,其在隔膜组织黏膜层表达明显。半定量检测结果显示CCR6和MIP⁃3α分子在隔膜组织黏膜层表达增多,与正常肠壁比较,差异有统计学意义(P=0.0027和P=0.0130)。结论在胚胎发育早期,隔膜组织黏膜层高表达MIP⁃3α和CCR6。本研究结果提示隔膜组织黏膜层内MIP⁃3α通过介导CCR6对树突状细胞和效应/记忆性T淋巴细胞产生选择性趋化作用,MIP⁃3α和CCR6的高表达介导了树突状细胞和效应/记忆性T淋巴细胞参与肠壁自身局部免疫应答和肠闭锁隔膜组织的发生。Objective To explore the expressions of chemokine receptor 6(CCR6)and macrophage inflammatory protein⁃3α(MIP⁃3α)in septum derived from type I intestinal atresia and normal intestinal wall.Methods Septum located in intestinal wall with a distance of<15 cm from Treitz ligament and normal intestinal wall around septum from the same patients were harvested for serial tissue sectioning and subsequent immunohistochemistry staining for histological observation of both CCR6 and MIP⁃3α.Results The expression of CCR6 was not detected in mucous of normal intestinal wall and it was present in septum of type I intestinal atresia.And the expression of MIP⁃3αwas positive in mucous of both normal intestinal wall and septum of type I intestinal atresia.Semi⁃quantitative comparison showed that significant elevations of CCR6 and MIP⁃3αin mucous of septum derived from type I intestinal atresia as compared with that in normal intestinal wall(P=0.0027 and 0.0130).Conclusion During an early phase of fetal development,CCR6 and MIP⁃3αwere up⁃regulated in mucosa of septum derived from type I intestinal atresia.And MIP⁃3αin septum derived from type I intestinal atresia induces chemotaxis of dendritic cell and effector/memory T lymphocyte through a up⁃regulation of CCR6.These pathways are probably involved in abnormal local immune response and formation of type I intestinal atresia.

关 键 词：受体 趋化因子 巨噬细胞炎性蛋白质类 小肠闭锁 

分 类 号：R726.5[医药卫生—儿科]