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作 者:刘凯[1] 李萌[1] 姬文晨[1] 杨卫周 孙小璐 LIU Kai;LI Meng;JI Wen-cheng;YANG Wei-zhou;SUN Xiao-lu(The First Affiliated Hospital of Xi'an Jiaotong University,Xi'an,Shaanri 710061,China)
机构地区:[1]西安交通大学第一附属医院骨科,陕西西安710061 [2]陕西省结核病防治研究所防治科,陕西西安710043
出 处:《中华医院感染学杂志》2023年第4期584-588,共5页Chinese Journal of Nosocomiology
基 金:陕西省重点研发计划基金资助项目(2020SF-080)。
摘 要:目的 探究肺炎克雷伯菌致慢性骨髓炎肿瘤坏死因子受体1(TNFR1)和炎症因子及其作用机制.方法 以肺炎克雷伯菌感染MC3T3-E1细胞为感染组,正常MC3T3-E1细胞做对照组,检测肺炎克雷伯菌感染前后细胞培养液TNFR1、C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)表达;采用流式细胞仪检测感染前后MC3T3-E1细胞凋亡情况;利用TNFR1阻断抗体孵育感染后的细胞,检测细胞上清液TN-FR1、CRP、TNF-α和IL-6水平,以验证TNFR1阻断抗体对肺炎克雷伯菌诱导的CRP、TNF-α和IL-6表达的抑制作用.结果 肺炎克雷伯菌感染MC3T3-E1细胞后,促进细胞凋亡,同时促进细胞TNFR1、CRP、TNF-α和IL-6表达;使用TNFR1阻断抗体孵育感染后的细胞,降低细胞TNFR1表达水平,同时抑制细胞CRP、TNF-α和IL-6的表达.结论 在肺炎克雷伯菌感染导致的慢性骨髓炎进展中TNFR1的表达正向调控了细胞炎症因子IL-6和TNF-α的表达.OBJECTIVE To investigate the changes in tumor necrosis factor receptor 1(TNFR1)and inflammatory factors in the progression of chronic osteomyelitis caused by Klebsiella pneumoniae and their mechanisms.METHODS Klebsiella pneumoniae infected MC3T3-El cells were used as the infection group,and normal MC3T3-El cells were used as the control group.The expression of TNFRl,C-reactive protein(CRP),tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in the cell culture medium before and after Klebsiella pneumoniae infection was detected.Flow cytometry was used to detect the apoptosis of MC3T3-El cells before and after infection.The infected cells were incubated with TNFR1 blocking antibody,and the levels of TNFRl,CRP,TNF-αand IL-6 in the cell supernatant were detected to verify the inhibitory effect of TNFR1 blocking antibody on the expression of CRP,TNF-αand IL-6 induced by Klebsiella pneumoniae.RESULTS After infection of MC3T3-El cells by Klebsiella pneumoniae,the apoptosis was promoted and the expression of TNFR1,CRP,TNF-αand IL-6 was increased.After incubation of infected cells with TNFR1 blocking antibody,the expression level of TNFR1 was reduced and the expression of CRP,TNF-αand IL-6 was inhibited.CONCLUSION The expression of TNFR1 positively regulated the expression of cellular inflammatory factors IL-6 and TNF-αin the progression of chronic osteomyelitis caused by Klebsiella pneumoniae infection.
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