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Salmonella-Induced Mucosal Lectin RegIII beta Kills Competing Gut Microbiota

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons81990

König,  Claudia
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons81995

Krah,  Alexander
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons81831

Bumann,  Dirk
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

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Volltexte (frei zugänglich)

PLoS_One_2011_6_e20749.pdf
(Verlagsversion), 2MB

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Zitation

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.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-BEF1-8
Zusammenfassung
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.