Gut inflammation provides a respiratory electron acceptor for Salmonella

Sebastian E. Winter, Parameth Thiennimitr, Maria G. Winter, Brian P. Butler, Douglas L. Huseby, Robert W. Crawford, Joseph M. Russell, Charles L. Bevins, L. Garry Adams, Renée M. Tsolis, John R. Roth and Andreas J. Bäumler ()
Additional contact information
Sebastian E. Winter: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Parameth Thiennimitr: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Maria G. Winter: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Brian P. Butler: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Douglas L. Huseby: University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Robert W. Crawford: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Joseph M. Russell: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Charles L. Bevins: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
L. Garry Adams: College of Veterinary Medicine, Texas A&M University
Renée M. Tsolis: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
John R. Roth: University of California, Davis, One Shields Avenue, Davis, California 95616, USA
Andreas J. Bäumler: School of Medicine, University of California, Davis, One Shields Avenue, Davis, California 95616, USA

Nature, 2010, vol. 467, issue 7314, 426-429

Abstract: Abstract Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for the biology of this diarrhoeal pathogen.

Date: 2010
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DOI: 10.1038/nature09415

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