诱发细胞自噬、抑制细胞凋亡是布鲁氏菌等胞内寄生菌造成持续性感染难以消灭的重要原因。前期研究发现：布鲁氏菌外膜蛋白OMP25能与宿主细胞FTH1蛋白发生互作，FTH1参与了布鲁氏菌诱发细胞自噬和抑制细胞凋亡的过程，但其如何对细胞自噬/凋亡信号通路调控的机理还不清楚。本项目拟①探讨布鲁氏菌omp25基因缺失株在体内、外对细胞自噬或凋亡的影响，②筛选并鉴定与FTH1互作的细胞因子，并验证这些相关细胞因子对宿主细胞自噬/凋亡信号通路的作用和功能，从分子、细胞和个体研究水平上，分析布鲁氏菌外膜蛋白OMP25和宿主细胞蛋白FTH1对自噬/凋亡信号通路的介导路径和调控机制，以期揭示布鲁氏菌与宿主细胞相互作用的重要机理，为阐明布鲁氏菌的发病机制提供理论依据。

Induced cell autophagy and inhibition of apoptosis are an important reason to cause intracellular bacterium such as Brucella hardly to be eliminated in persistent infection.We Funded that host cell factor FTH1 interacts with Brucella outer membrane protein OMP25, and plays an important role in the inhibition of apoptosis in Brucella. Here we will study deeply on regulatory mechanism of host cell autophagy/apoptosis signaling pathway by OMP25 and FTH1. The project is planned to constuct Brucella omp25 gene deletion strains to the impact on autophagy or apoptosis, screening and identifying cytokines interacted with the FTH1 ,which related with autophagy/apoptosis. we verify the function of these cytokines as main research , compare the effect of the Brucella outer membrane protein OMP25 and host cytokines FTH1 on host cells autophagy/apoptosis signaling pathway, analysis its mechanism From the molecular, cellular, individual level. The study reveals an important mechanism of Brucella interaction with host cells, and provide a theoretical basis to clarify the pathogenesis of Brucella.