The Potassium Transporter Trk and External Potassium Modulate Salmonella enterica Protein Secretion and Virulence

被引:62
作者
Su, Jing [1 ,2 ]
Gong, Hao [1 ]
Lai, Jeff [1 ]
Main, Andrew [1 ]
Lu, Sangwei [1 ]
机构
[1] Univ Calif Berkeley, Sch Publ Hlth, Program Infect Dis & Immun, Berkeley, CA 94720 USA
[2] Nanjing Univ, Sch Life Sci, Dept Biosci & Technol, Nanjing 210008, Jiangsu, Peoples R China
关键词
KDP OPERON EXPRESSION; ESCHERICHIA-COLI; TYPHIMURIUM INVASION; K+ UPTAKE; TRANSCRIPTIONAL REGULATION; CHROMOSOMAL GENES; GLOBAL REGULATOR; RESISTANCE; SYSTEM; CELLS;
D O I
10.1128/IAI.01027-08
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:667 / 675
页数:9
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