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Cell Host Microbe. 2013 Dec 11;14(6):641-51. doi: 10.1016/j.chom.2013.11.002.

Microbiota-derived hydrogen fuels Salmonella typhimurium invasion of the gut ecosystem.

Author information

1
Institute of Microbiology, ETH Zürich, CH-8093 Zurich, Switzerland.
2
SIB Swiss Institute of Bioinformatics, University of Zurich, CH-8057 Zurich, Switzerland.
3
Max-von-Pettenkofer Institute, Ludwig-Maximilians-Universität Munich, 80336 Munich, Germany.
4
Department of Environmental Microbiology, Eawag and Department of Environmental Systems Sciences, ETH Zurich, CH-8600 Dübendorf, Switzerland.
5
Institute of Microbiology, ETH Zürich, CH-8093 Zurich, Switzerland. Electronic address: wolf-dietrich.hardt@micro.biol.ethz.ch.

Abstract

The intestinal microbiota features intricate metabolic interactions involving the breakdown and reuse of host- and diet-derived nutrients. The competition for these resources can limit pathogen growth. Nevertheless, some enteropathogenic bacteria can invade this niche through mechanisms that remain largely unclear. Using a mouse model for Salmonella diarrhea and a transposon mutant screen, we discovered that initial growth of Salmonella Typhimurium (S. Tm) in the unperturbed gut is powered by S. Tm hyb hydrogenase, which facilitates consumption of hydrogen (H2), a central intermediate of microbiota metabolism. In competitive infection experiments, a hyb mutant exhibited reduced growth early in infection compared to wild-type S. Tm, but these differences were lost upon antibiotic-mediated disruption of the host microbiota. Additionally, introducing H2-consuming bacteria into the microbiota interfered with hyb-dependent S. Tm growth. Thus, H2 is an Achilles' heel of microbiota metabolism that can be subverted by pathogens and might offer opportunities to prevent infection.

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PMID:
24331462
DOI:
10.1016/j.chom.2013.11.002
[Indexed for MEDLINE]
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