Su Jing, Gong Hao, Lai Jeff, Main Andrew, Lu Sangwei
Program in Infectious Diseases and Immunity, School of Public Health, University of California, Berkeley, California 94720-7354, USA.
Infect Immun. 2009 Feb;77(2):667-75. doi: 10.1128/IAI.01027-08. Epub 2008 Nov 10.
Potassium (K(+)) is the most abundant intracellular cation and is essential for many physiological functions of all living organisms; however, its role in the pathogenesis of human pathogens is not well understood. In this study, we characterized the functions of the bacterial Trk K(+) transport system and external K(+) in the pathogenesis of Salmonella enterica, a major food-borne bacterial pathogen. Here we report that Trk is important for Salmonella to invade and grow inside epithelial cells. It is also necessary for the full virulence of Salmonella in an animal infection model. Analysis of proteins of Salmonella indicated that Trk is involved in the expression and secretion of effector proteins of the type III secretion system (TTSS) encoded by Salmonella pathogenicity island 1 (SPI1) that were previously shown to be necessary for Salmonella invasion. In addition to the role of the Trk transporter in the pathogenesis of Salmonella, we discovered that external K(+) modulates the pathogenic properties of Salmonella by increasing the expression and secretion of effector proteins of the SPI1-encoded TTSS and by enhancing epithelial cell invasion. Our studies demonstrated that K(+) is actively involved in the pathogenesis of Salmonella and indicated that Salmonella may take advantage of the high K(+) content inside host cells and in the intestinal fluid during diarrhea to become more virulent.
钾离子（K⁺）是细胞内最丰富的阳离子，对所有生物体的许多生理功能至关重要；然而，其在人类病原体发病机制中的作用尚未得到充分了解。在本研究中，我们对肠道沙门氏菌（一种主要的食源性病原体）发病机制中细菌Trk钾离子转运系统和胞外钾离子的功能进行了表征。在此我们报告，Trk对沙门氏菌侵入上皮细胞并在其中生长很重要。在动物感染模型中，它对沙门氏菌的完全毒力也是必需的。对沙门氏菌蛋白质的分析表明，Trk参与了由沙门氏菌致病岛1（SPI1）编码的III型分泌系统（TTSS）效应蛋白的表达和分泌，先前已证明这些效应蛋白对沙门氏菌的侵入是必需的。除了Trk转运蛋白在沙门氏菌发病机制中的作用外，我们还发现胞外钾离子通过增加SPI1编码的TTSS效应蛋白的表达和分泌以及增强上皮细胞侵袭来调节沙门氏菌的致病特性。我们的研究表明，钾离子积极参与沙门氏菌的发病机制，并表明沙门氏菌可能利用宿主细胞内以及腹泻时肠液中的高钾离子含量来变得更具毒性。
