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dc.contributor.author
Stecher, Baerbel
dc.contributor.author
Robbiani, Riccardo
dc.contributor.author
Walker, Alan W.
dc.contributor.author
Westendorf, Astrid M.
dc.contributor.author
Barthel, Manja
dc.contributor.author
Kremer, Marcus
dc.contributor.author
Chaffron, Samuel
dc.contributor.author
Macpherson, Andrew J.
dc.contributor.author
Buer, Jan
dc.contributor.author
Parkhill, Julian
dc.contributor.author
Dougan, Gordon
dc.contributor.author
von Mering, Christian
dc.contributor.author
Hardt, Wolf-Dietrich
dc.date.accessioned
2019-06-05T15:52:32Z
dc.date.available
2017-06-08T17:24:35Z
dc.date.available
2019-06-05T15:52:32Z
dc.date.issued
2007-08-28
dc.identifier.issn
1544-9173
dc.identifier.issn
1545-7885
dc.identifier.other
10.1371/journal.pbio.0050244
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/6404
dc.identifier.doi
10.3929/ethz-b-000006404
dc.description.abstract
Most mucosal surfaces of the mammalian body are colonized by microbial communities (“microbiota”). A high density of commensal microbiota inhabits the intestine and shields from infection (“colonization resistance”). The virulence strategies allowing enteropathogenic bacteria to successfully compete with the microbiota and overcome colonization resistance are poorly understood. Here, we investigated manipulation of the intestinal microbiota by the enteropathogenic bacterium Salmonella enterica subspecies 1 serovar Typhimurium (S. Tm) in a mouse colitis model: we found that inflammatory host responses induced by S. Tm changed microbiota composition and suppressed its growth. In contrast to wild-type S. Tm, an avirulent invGsseD mutant failing to trigger colitis was outcompeted by the microbiota. This competitive defect was reverted if inflammation was provided concomitantly by mixed infection with wild-type S. Tm or in mice (IL10−/−, VILLIN-HACL4-CD8) with inflammatory bowel disease. Thus, inflammation is necessary and sufficient for overcoming colonization resistance. This reveals a new concept in infectious disease: in contrast to current thinking, inflammation is not always detrimental for the pathogen. Triggering the host's immune defence can shift the balance between the protective microbiota and the pathogen in favour of the pathogen.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Public Library of Science
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/3.0/
dc.title
Salmonella enterica serovar typhimurium exploits inflammation to compete with the intestinal microbiota
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 3.0 Unported
ethz.journal.title
PLoS Biology
ethz.journal.volume
5
en_US
ethz.journal.issue
10
en_US
ethz.journal.abbreviated
PLoS biol.
ethz.pages.start
2177
en_US
ethz.pages.end
2189
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.nebis
004606893
ethz.publication.place
Lawrence, KS
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02520 - Institut für Mikrobiologie / Institute of Microbiology::03589 - Hardt, Wolf-Dietrich / Hardt, Wolf-Dietrich
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02520 - Institut für Mikrobiologie / Institute of Microbiology::03589 - Hardt, Wolf-Dietrich / Hardt, Wolf-Dietrich
ethz.date.deposited
2017-06-08T17:24:56Z
ethz.source
ECIT
ethz.identifier.importid
imp59364ba0a125533740
ethz.ecitpid
pub:16811
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-26T22:12:33Z
ethz.rosetta.lastUpdated
2020-02-15T19:26:20Z
ethz.rosetta.versionExported
true
ethz.COinS
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