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  Salmonella-Induced Mucosal Lectin RegIII beta Kills Competing Gut Microbiota

Stelter, C., Käppeli, R., König, C., Krah, A., Hardt, W.-D., Stecher, B., et al. (2011). Salmonella-Induced Mucosal Lectin RegIII beta Kills Competing Gut Microbiota. PLoS ONE, 6(6): e20749. doi:10.1371/journal.pone.0020749.

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Genre: Journal Article
Alternative Title : PLoS One

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PLoS_One_2011_6_e20749.pdf (Publisher version), 2MB
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© 2011 Stelter et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
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 Creators:
Stelter, Christian, Author
Käppeli, Rina, Author
König, Claudia1, Author              
Krah, Alexander1, Author              
Hardt, Wolf-Dietrich, Author
Stecher, Bärbel, Author
Bumann, Dirk1, Author              
Affiliations:
1Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society, ou_1664147              

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 Abstract: Intestinal inflammation induces alterations of the gut microbiota and promotes overgrowth of the enteric pathogen Salmonella enterica by largely unknown mechanisms. Here, we identified a host factor involved in this process. Specifically, the C-type lectin RegIII beta is strongly upregulated during mucosal infection and released into the gut lumen. In vitro, RegIII beta kills diverse commensal gut bacteria but not Salmonella enterica subspecies I serovar Typhimurium (S. Typhimurium). Protection of the pathogen was attributable to its specific cell envelope structure. Co-infection experiments with an avirulent S. Typhimurium mutant and a RegIII beta-sensitive commensal E. coli strain demonstrated that feeding of RegIII beta was sufficient for suppressing commensals in the absence of all other changes inflicted by mucosal disease. These data suggest that RegIII beta production by the host can promote S. Typhimurium infection by eliminating inhibitory gut microbiota.

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Language(s): eng - English
 Dates: 2011-06-09
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 572773
ISI: 000291612900022
DOI: 10.1371/journal.pone.0020749
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Title: PLoS ONE
  Alternative Title : PLoS One
Source Genre: Journal
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Publ. Info: SAN FRANCISCO : PUBLIC LIBRARY SCIENCE
Pages: - Volume / Issue: 6 (6) Sequence Number: e20749 Start / End Page: - Identifier: ISSN: 1932-6203