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作 者:袁喆晨 汪林芳 苏芬芬 凌晓晶 陈时豪 曹佳泽 方倩 朴正浩 YUAN Zhechen;WANG Linfang;SU Fenfen;LING Xiaojing;CHEN Shihao;CAO Jiaze;FANG Qian;PIAO Zhenghao(School of Medicine,Hangzhou Normal University,Hangzhou 311121,China)
出 处:《杭州师范大学学报(自然科学版)》2020年第3期317-322,共6页Journal of Hangzhou Normal University(Natural Science Edition)
基 金:杭州市科技委项目(20180533B28);杭州师范大学本科生创新能力提升工程项目.
摘 要:为研究自噬在绿脓杆菌感染时对中性粒细胞募集的作用,在分离小鼠骨髓中性粒细胞后进行了中性粒细胞募集级联反应中的粘附实验.结果表明,绿脓杆菌感染可引起中性粒细胞的粘附,同时伴随着整合素CD11b/CD18的表达增强.免疫印迹实验发现,绿脓杆菌感染时中性粒细胞的自噬标志蛋白LC3-II的表达增加,而在自噬抑制剂3-甲基腺苷处理时LC3-II的表达显著地被抑制.3-甲基腺苷还可以显著地抑制中性粒细胞的粘附和整合素CD11b的表达,但是CD18的表达未受抑制剂的影响.由此确定,在绿脓杆菌感染时自噬对骨髓中性粒细胞的粘附起促进作用,这一过程与整合素CD11b的激活相伴.To investigate the effects of autophagy on neutrophils recruitment during Pseudomonas aeruginosainfection,neutrophils were isolated from the bone marrow of mice,and the adhesion experiment in neutrophil recruitment cascade reaction was performed.The results showed that P.aeruginosainfection could induce neutrophils adhesion and activate integrin CD11 b/CD18.Western blotting revealed that the expression of autophagic marker protein LC3-II in neutrophils increased at the time of P.aeruginosa infection,while the expression of LC3-II was significantly inhibited during the treatment with autophagy inhibitor 3-methyladenosine.3-MA also obviously inhibited the adhesion and expression of integrin CD11 bof neutrophils,but CD18 was not affected.It was indicated that autophagy promoted the adhesion of neutrophils during P.aeruginosainfection,and this process went hand in hand with the activation of integrin CD11 b.
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