Salmonella-Host Cell Interactions

肠炎沙门氏菌血清型鼠伤寒沙门氏菌是人类肠结肠炎最常见的病因之一。这种兼性细胞内病原体的发病机制依赖于侵入非吞噬细胞的能力，如在肠上皮中发现的细胞。侵袭依赖于III型分泌系统（T3SS1），该系统用于将一组细菌效应蛋白转运到宿主细胞中。内化后，胞内沙门氏菌在经过修饰的吞噬体中存活并复制，即含沙门氏菌液泡（SCV）。第二种III型系统（T3SS2）是在细胞内诱导的，与细胞内存活/复制和SCV的生物发生有关。为了了解沙门氏菌的发病机制，我们必须剖析单个T3SS1和T3SS2效应蛋白的作用，以及控制它们在宿主细胞内表达和活性的机制。

Salmonella enterica serovar Typhimurium is one of the most common causes of enterocolitis in humans. Pathogenesis of this facultative intracellular pathogen is dependent on the ability to invade non-phagocytic cells, such as those found in the intestinal epithelium. Invasion is dependent on a type III secretion system (T3SS1), which is used to translocate a set of bacterial effector proteins into the host cell. Following internalization intracellular Salmonella survive and replicate within a modified phagosome, the Salmonella-containing vacuole (SCV). A second type III system (T3SS2) is induced intracellularly and is associated with intracellular survival/replication and biogenesis of the SCV. To understand Salmonella pathogenesis we must dissect the roles of the individual T3SS1 and T3SS2 effector proteins as well as the mechanisms that control their expression and activity inside host cells.