NLRP3炎症小体在牛种布鲁氏菌2308和RB51侵染人巨噬细胞THP-1过程中作用的初步研究

Preliminary Study on the Role of the NLRP3-Inflammasome during the Infection of the Human Macrophages THP-1 by the Brucella abortus 2308 and RB51

为了探索NLRP3炎症小体在布鲁氏菌侵染宿主细胞过程中的作用,以牛种布鲁氏菌强毒株2308、弱毒株RB51侵染人巨噬细胞THP-1,用实时荧光定量PCR方法探索布鲁氏菌引起宿主细胞中NLRP3炎症小体及相关细胞因子的变化情况。结果表明:在布鲁氏菌侵染THP-1细胞后0-24 h,NLRP3炎症小体在转录水平上总体呈现先下降后上升的趋势,THP-1细胞形态随着侵染时间的延长变得不规则,且出现聚集现象。强毒株2308对NLRP3炎症小体相关基因转录水平和THP-1细胞形态变化的影响均强于弱毒株RB51。这表明布鲁氏菌在感染初期有短暂抑制炎症小体的能力,这可能是布鲁氏菌逃避巨噬细胞杀灭作用的一种策略。

In order to research the function of the NLRP3-inflammasome in the host cell infected by Brucella,the human macrophages THP-1 was infected by the Brucella abortus virulent strain 2308 and the low virulent strain RB51,which were used to explore the change of NLRP3-inflammasome and its related eytokines at transcription level by quantitative Real-time PCR method.The results showed that the general transcription level of NLRP3-inflammasome in THP-1 infected by Brucella during 0 h to 24 h was decreased at first and then increased.THP-1 cells became irregular and gathered together with the time elongation after infected by the Brucella.2308 had a greater impact on both the change in transcription of NLRP3- inflammasome and the cell appearance than RB 5.1.This study indicated that the Brucella has ability to shortly inhibit NLRP3-inflammasome at the beginning of infection.It may be a strategy for Brucella to avoid being killed by the macrophages.