IRF3在绿脓杆菌感染时抑制中性粒细胞粘附的机制研究  

Molecular Mechanisms of IRF3 Inhibit Neutrophils Adhesion Infected with Pseudomonas aeruginosa

作　　者：汪林芳 袁喆晨 苏芬芬 凌晓晶 黄小园 李婷 朴正浩 WANG Linfang;YUAN Zhechen;SU Fenfen;LING Xiaojing;HUANG Xiaoyuan;LI Ting;PIAO Zhenghao(School of Medicine,Hangzhou Normal University,Hangzhou 311121,China;Hangzhou Medical College,Hangzhou 311399,China)

机构地区：[1]杭州师范大学医学院,浙江杭州311121 [2]杭州医学院,浙江杭州311399

出　　处：《杭州师范大学学报（自然科学版）》2019年第5期516-520,共5页Journal of Hangzhou Normal University(Natural Science Edition)

基　　金：杭州市科技委基金项目(20180533B28);杭州师范大学“本科生创新能力提升工程项目”

摘　　要：干扰素调节因子3(interferon regulatory factor 3,IRF3)能抑制小鼠中性粒细胞的募集.为了研究其机制,分离小鼠骨髓中性粒细胞进行研究,发现在绿脓杆菌感染时IRF3抑制中性粒细胞的粘附.整合素是中性粒细胞执行功能的重要分子,IRF3能显著地抑制CD11b的表达.进行免疫印迹实验没有检测到Akt的Ser473和Thr308位点的磷酸化,但发现IRF3抑制Akt蛋白的表达.还发现Wortmannin显著地抑制中性粒细胞的粘附和CD11b的表达.由此确定,IRF3抑制中性粒细胞的粘附与整合素CD11b的表达密切相关,而Wortmannin是重要的抑制剂.可以推测,IRF3可能通过抑制Akt蛋白的稳定而调节中性粒细胞的功能.研究结果将为IRF3在绿脓杆菌感染时抑制中性粒细胞募集的分子机制研究指明方向.Interferon regulatory factor 3(IRF3)inhibits the recruitment of mice neutrophils.In order to study the mechanism,the neutrophils are isolated from bone marrow,it is found that IRF3 inhibits neutrophils adhesion infected with P.aeruginosa.Integrin is an important molecule for the activation of neutrophils,IRF3 significantly inhibits the expression of CD11b.The phosphorylation of Akt(Ser473 and Thr308)does not detected,but it is found that IRF3 can inhibit Akt expression.And the neutrophils adhesion and integrin CD11b are significantly inhibited by Wortmannin.Thus,the inhibition of neutrophil adhesion by IRF3 is closely involved in CD11b expression,and Wortmanninis an important inhibitor.It can be speculated that IRF3 regulates the neutrophils function by the stabilization of Akt.These results indicate the direction for study the molecular mechanism of IRF3 regulates neutrophils recruitment infected with P.aeruginosa.

关 键 词：干扰素调节因子3 中性粒细胞 粘附 整合素 AKT 

分 类 号：R3[医药卫生—基础医学]