Gut inflammation provides a respiratory electron acceptor for Salmonella.
Nature. 2010 Sep 23; 467(7314):426-9
Nizet V: F1000Prime Recommendation of [Winter SE et al., Nature 2010, 467(7314):426-9]. In F1000Prime, 29 Sep 2010; DOI: 10.3410/f.5337958.5293054. F1000Prime.com/5337958#eval5293054
Khosravi-Far R and Kurakin A: F1000Prime Recommendation of [Winter SE et al., Nature 2010, 467(7314):426-9]. In F1000Prime, 11 Oct 2010; DOI: 10.3410/f.5337958.5434054. F1000Prime.com/5337958#eval5434054
Alpers D: F1000Prime Recommendation of [Winter SE et al., Nature 2010, 467(7314):426-9]. In F1000Prime, 15 Oct 2010; DOI: 10.3410/f.5337958.5591060. F1000Prime.com/5337958#eval5591060
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F1000Prime Recommendations, Dissents and Comments for [Winter SE et al., Nature 2010, 467(7314):426-9]. In F1000Prime, 10 Dec 2013; F1000Prime.com/5337958
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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.
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