病原菌与宿主的相互作用是决定其感染和发病的前提。类鼻疽菌作为一种严重威胁人类健康和危害公共生物安全的热带医学传染病病原，有效逃逸宿主免疫细胞吞噬溶酶体的清除作用是其致病的关键，而类鼻疽菌的三型分泌系统（T3SS）在此过程中发挥了重要的调控作用。本课题组前期通过基因敲除、芯片筛选和功能验证发现：类鼻疽菌感染宿主细胞后利用T3SS效应蛋白BapC干扰Rab7功能阻碍宿主细胞吞噬囊泡转运成熟的过程，但具体分子机制未明。本项目拟在类鼻疽菌感染的巨噬细胞模型中，利用激光共聚焦、Western blot等观察BapC介导的吞噬囊泡转运成熟障碍在类鼻疽菌逃逸宿主免疫清除中的作用，同时利用Pull down、Co-IP、质谱分析等探究BapC是通过何种手段和途径来干扰Rab7调控吞噬囊泡转运成熟的，以期为寻找类鼻疽菌新的有效的防治策略提供理论指导。

The interaction between the pathogens and the host cells is the premise to determine its infection and disease. Burkholderia pseudomalle, which is endemic across tropical regions, is a serious threat to human health and public biosafety. B. pseudomalle, a facultative intracellular pathogen, is very successful at survival in vivo, in mainly part due to its various virulence factors for host cell invasion and escape from the endocytic vacuole in to the cytosol. Numerous studies have indicated the Type III Secretion Systems (T3SSs), especially T3SS-3, is of great importance for B. pseudomallei to efficiently escape the endocytic vesicle, but the detailed mechanisms remain unknown. In the present study, we found that the effector protein BapC of T3SS-3 prevents the localization of Rab7 to B. pseudomallei-containing vacuole (BCV), resulting in disturbing the phagosome maturation. Based on these preliminary results, the aim of this project is to define the specific interactions between B. pseudomallei and macrophage to elucidate the detailed molecular mechanisms by which B. pseudomallei BapC targets Rab7 to interfere with the BCV trafficking to escape lysosome-mediated killing during the later stage of phagocytosis. This work will lay the groundwork for strategies aimed at combating the infectious disease, and may provide useful information for developing potential therapeutic interventions against B. pseudomallei.