抑制细胞凋亡是细菌胞内寄生的重要策略，细胞转录因子NF-κB与细胞凋亡关系密切，参与多种凋亡相关基因的转录调控。课题组前期研究表明：布鲁氏菌感染细胞过程中能抑制宿主细胞凋亡，布鲁氏菌强毒株比弱毒株表现出更强的抑制作用；布鲁氏菌感染宿主细胞能激活NF-κB，强毒株比弱毒株激活NF-κB水平低。目前布鲁氏菌感染宿主细胞的过程中NF-κB如何调控细胞凋亡信号通路的机制还不完全清楚。本项目拟在现有工作基础上，基于布鲁氏菌感染细胞过程，探讨布鲁氏菌激活NF-κB与细胞凋亡的关系，采用比较转录组学、蛋白组学、CHIP-seq等技术筛选并鉴定布鲁氏菌强/弱毒株感染宿主细胞过程中NF-κB转录调控的细胞凋亡相关靶基因，研究其生物学功能，阐明靶基因参与调控的细胞凋亡信号通路，揭示布鲁氏菌强/弱毒株激活NF-κB与抑制细胞凋亡作用的分子机制，为进一步阐明布鲁氏菌病致病机制提供理论依据。

Inhibition of cell apoptosis is an important strategy for bacterial intracellular Survival and reproduction. Cell transcription factor NF- kappa B is closely related to apoptosis, and is involved in the transcriptional regulation of many apoptosis related genes. Our previous studies showed that Brucella infection can inhibit host cell apoptosis, and Brucella virulent strain showed stronger inhibition than attenuated strain. Brucella infected host cells could activate NF- kappa B, but strong virulent strain had lower activation level of NF- kappa B than virulent strain. Now, It is not clear how NF- kappa B regulates the apoptosis signaling pathway during the infection of the host cells of Brucella.This project is on the basis of existing work, starting from the Brucella infection cells process, to explore the relationship between activation of NF- kappa B and cell apoptosis, comparative transcriptomics, proteomics, CHIP-seq screening and identification of Brucella virulent / attenuated strain infection on host cell in the process of NF- kappa B transcriptional regulation of the target gene of cell apoptosis, and study and analysis its biological function, apoptosis signaling pathways involved in the regulation of target genes to clarify the molecular mechanisms underlying the Brucella strains of virulent / attenuated activation of NF- kappa B and inhibit the cell apoptosis. It will provide a theoretical basis for elucidating the pathogenesis of Brucellosis.