Salmonella-Host Cell Interactions

沙门氏菌-宿主细胞相互作用

• 批准号: 8157093
• 负责人: Olivia Steele-Mortimer
• 金额: $ 91.16万
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8157093
• 关键词: Cell Communication; Salmonella

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. Since the expression and function of these virulence factors is exquisitely dependent on the intracellular environment, we are focusing on developing appropriate in vitro systems to study their activities at the molecular level.

沙门氏菌血清鼠伤寒是人类小肠结肠炎的最常见原因之一。这种夫妇的细胞内病原体的发病机制取决于侵入非吞噬细胞的能力，例如在肠上皮中发现的细胞。入侵取决于III型分泌系统（T3SS1），该系统用于将一组细菌效应子蛋白转移到宿主细胞中。内在化后，细胞内沙门氏菌在含沙门氏菌的液泡（SCV）中生存并复制。第二型III系统（T3SS2）是细胞内诱导的，与SCV的细胞内存活/复制和生物发生有关。要了解沙门氏菌的发病机理，我们必须剖析单个T3SS1和T3SS2效应蛋白的作用，以及控制其在宿主细胞内表达和活性的机制。由于这些毒力因子的表达和功能非常取决于细胞内环境，因此我们着重于开发适当的体外系统来研究其在分子水平上的活性。