Hallstrom Kelly N, McCormick Beth A
a Department of Microbiology and Physiological Systems , University of Massachusetts Medical School , Worcester , MA , USA.
Gut Microbes. 2016;7(2):136-45. doi: 10.1080/19490976.2015.1128626.
Salmonella enterica Typhimurium employs type III secreted effectors to induce cellular invasion and pathogenesis. We previously reported the secreted effector SipA is in part responsible for inducing the apical accumulation of the host membrane protein PERP, a host factor we have shown is key to the inflammatory response induced by Salmonella. We now report that the S. Typhimurium type III secreted effector SipC significantly contributes to PERP redistribution to the apical membrane surface. To our knowledge, this is the first report demonstrating a role for SipC in directing the trafficking of a host membrane protein to the cell surface. In sum, facilitation of PERP trafficking appears to be a result of type III secreted effector-mediated recruitment of vesicles to the apical surface. Our study therefore reveals a new role for SipC, and builds upon previous reports suggesting recruitment of vesicles to the cell surface is important for Salmonella invasion.
鼠伤寒沙门氏菌利用III型分泌效应蛋白来诱导细胞侵袭和发病机制。我们之前报道过，分泌效应蛋白SipA部分负责诱导宿主膜蛋白PERP在顶端积累，我们已经证明PERP是沙门氏菌诱导炎症反应的关键宿主因子。我们现在报道，鼠伤寒沙门氏菌III型分泌效应蛋白SipC对PERP重新分布到顶端膜表面有显著作用。据我们所知，这是首次报道SipC在指导宿主膜蛋白向细胞表面运输中发挥作用。总之，促进PERP运输似乎是III型分泌效应蛋白介导的囊泡向顶端表面募集的结果。因此，我们的研究揭示了SipC的新作用，并基于之前的报道，即囊泡向细胞表面的募集对沙门氏菌入侵很重要。
