Interactions between Salmonella enterica and its intracellular habitat

细胞内生存和复制是肠出血性沙门氏菌重要的毒力表型，需要多种毒力因子的协同作用。最近的工作表明，沙门氏菌可以积极地调节含有沙门氏菌的囊泡的生物发生，例如通过避免将具有抗菌活性的囊泡输送到这个隔室，以及通过吸引可能促进细胞内增殖的内噬菌体。我们观察到，细胞内沙门氏菌利用III型分泌系统将效应蛋白转移到受感染的宿主细胞中，并有助于保护宿主免受抗菌活动的影响。在这个项目中，将分析这种对宿主细胞的操纵的分子机制。将研究细胞内沙门氏菌调节宿主细胞以获得允许复制和缺乏杀菌防御机制的囊泡的机制。将特别强调由沙门氏菌致病岛2编码的III型分泌系统转位的效应蛋白的作用。在拟议的项目中，研究了各种效应蛋白的转位、亚细胞定位以及与宿主细胞分子的相互作用。

Intracellular survival and replication is an important virulence phenotype of Salmonella enterica and requires the coordinate function of several virulence factors. Recent work indicates that Salmonella can actively modulate the biogenesis of the Salmonella-containing vesicle, e.g. by avoidance of delivery of encymes with antimicrobial activity to this compartment as well as by attraction of endosomes that may promote intracellular proliferation. We observed that intracellular Salmonella employ a type III secretion system that translocates effector proteins into infected host cells and contributes to the protection against antimicrobial activities of the host. In this project, the molecular mechanisms of this manipulation of the host cell will be analyzed. The mechanisms will be studied by which intracellular Salmonella can modulate their host cell in order to achieve a vesicle that is permissive for replication and devoid of bacteriocidal defense mechanisms. Special emphasis will be given to the role of effector proteins that are translocated by a type III secretion system encoded by Salmonella Pathogenicity Island 2. In the proposed project, the translocation, subcellular localization and interaction with host cell molecules of various effector proteins is investigated.