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Infection and Immunity, February 2009, p. 667-675, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.01027-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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

Jing Su,1,2 Hao Gong,1 Jeff Lai,1 Andrew Main,1 and Sangwei Lu1*

Program in Infectious Diseases and Immunity, School of Public Health, University of California, Berkeley, California 94720,1 Department of Bioscience and Technology, School of Life Science, Nanjing University, Nanjing, Jiangsu, People's Republic of China2

Received 18 August 2008/ Returned for modification 17 September 2008/ Accepted 31 October 2008

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.

* Corresponding author. Mailing address: 16 Barker Hall, University of California, Berkeley, CA 94720-7354. Phone: (510) 643-4986. Fax: (510) 643-9955. E-mail: sangwei{at}berkeley.edu

{triangledown} Published ahead of print on 10 November 2008.

Editor: A. J. Bäumler

Infection and Immunity, February 2009, p. 667-675, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.01027-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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