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作 者:何小丽 吴林青[1] 许伟群 郑晨华 傅冷西[2] 章涛[1] HE Xiaoli;WU Linqing;XU Weiqun;ZHENG Chenhua;FU Lengxi;ZHANG Tao(School of Basic Medical Sciences,Fujian Medical University,Fuzhou 350122,China;Fujian Platform for Medical Research,The First Affiliated Hospital of Fujian Medical University,Fuzhou 350005,China)
机构地区:[1]福建医科大学基础医学院,福州350122 [2]福建省临床医学实验平台,福建医科大学附属第一医院,福州350005
出 处:《福建医科大学学报》2018年第4期215-219,共5页Journal of Fujian Medical University
基 金:福建省临床医学实验平台资助项目(FYKFKT-201702)
摘 要:目的研究白细胞介素33敲除(IL-33-/-)小鼠腹腔巨噬细胞(pMφ)表面分子表达及炎性因子分泌水平的变化,探讨IL-33-/-对pMφ极化的影响。方法收集C57BL/6IL-33-/-小鼠和野生型(WT)小鼠的pMφ,体外培养48h后,分为IL-33-/-组和WT组,比较2组小鼠pMφ炎性介质、细胞因子及表面分子表达水平的变化。结果 IL-33-/-小鼠pMφM1型标志物NO,MHCⅡ类分子,TLR4及CD86的表达水平均高于WT小鼠(NO,CD86和MHCⅡ,P<0.01;TLR4,P<0.05)。结论 IL-33-/-可促进小鼠pMφ向M1型极化。Objective To investigate the effect of interleukin-33 defect on the polarization of peritoneal macrophages with the expressions of surface and inflammatory molecules from IL-33 knockout(IL-33-/-)mice. Methods pMφwas isolated from C57BL/6 wild type(WT)and IL-33-/-mice and divided into IL-33-/-group and WT group,then cultured in vitro for 48 hours;the mRNA of iNOS,Arg-1,IL-1,IL-10 and IL-12 were detected by real-time PCR. The secretion of IL-12,TNF-α,IL-10 and NO were detected by ELISA and Griess method respectively. The surface molecules(CD80,CD86,CD206,TLR4,TLR2,MHCⅡ)were analyzed by flow cytometry. Results The expression of M1 marks(NO,MHCⅡand CD86)were increased(P<0.01)in IL-33-/-mice compared with WT group;the expression of TLR4 in pMφfrom mice IL-33-/-group was higher than WT group(P<0.05). Conclusion The peritoneal macrophages were polarized to M1 direction in IL-33-/-mice.
分 类 号:R329.24[医药卫生—人体解剖和组织胚胎学]
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