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dc.contributor.author
Huang, Yen-Lin
dc.contributor.author
Chassard, Christophe
dc.contributor.author
Hausmann, Martin
dc.contributor.author
Von Itzstein, Mark
dc.contributor.author
Hennet, Thierry
dc.date.accessioned
2018-09-12T11:20:38Z
dc.date.available
2017-06-11T19:06:31Z
dc.date.available
2018-09-12T11:20:38Z
dc.date.issued
2015
dc.identifier.other
10.1038/ncomms9141
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/103748
dc.identifier.doi
10.3929/ethz-b-000103748
dc.description.abstract
Rapid shifts in microbial composition frequently occur during intestinal inflammation, but the mechanisms underlying such changes remain elusive. Here we demonstrate that an increased caecal sialidase activity is critical in conferring a growth advantage for some bacteria including Escherichia coli (E. coli) during intestinal inflammation in mice. This sialidase activity originates among others from Bacteroides vulgatus, whose intestinal levels expand after dextran sulphate sodium administration. Increased sialidase activity mediates the release of sialic acid from intestinal tissue, which promotes the outgrowth of E. coli during inflammation. The outburst of E. coli likely exacerbates the inflammatory response by stimulating the production of pro-inflammatory cytokines by intestinal dendritic cells. Oral administration of a sialidase inhibitor and low levels of intestinal α2,3-linked sialic acid decrease E. coli outgrowth and the severity of colitis in mice. Regulation of sialic acid catabolism opens new perspectives for the treatment of intestinal inflammation as manifested by E. coli dysbiosis.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Nature Publishing Group
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.title
Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2015-08-25
ethz.journal.title
Nature Communications
ethz.journal.volume
6
en_US
ethz.pages.start
8141
en_US
ethz.size
11 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.grant
The Microbe-Host Interface: Molecular Mechanisms Mediating Protective and Pathological Innate and Adaptive Immune Responses within the Gut
en_US
ethz.identifier.wos
ethz.identifier.nebis
007044158
ethz.publication.place
London
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02070 - Dep. Gesundheitswiss. und Technologie / Dep. of Health Sciences and Technology::02701 - Inst.f. Lebensmittelwiss.,Ernährung,Ges. / Institute of Food, Nutrition, and Health::03626 - Lacroix, Christophe / Lacroix, Christophe
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02070 - Dep. Gesundheitswiss. und Technologie / Dep. of Health Sciences and Technology::02701 - Inst.f. Lebensmittelwiss.,Ernährung,Ges. / Institute of Food, Nutrition, and Health::03626 - Lacroix, Christophe / Lacroix, Christophe
ethz.grant.agreementno
154488
ethz.grant.fundername
SNF
ethz.grant.funderDoi
10.13039/501100001711
ethz.grant.program
ethz.date.deposited
2017-06-11T19:06:44Z
ethz.source
ECIT
ethz.identifier.importid
imp5936536f06dec37717
ethz.ecitpid
pub:162148
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-13T07:52:14Z
ethz.rosetta.lastUpdated
2019-02-03T07:54:03Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.atitle=Sialic%20acid%20catabolism%20drives%20intestinal%20inflammation%20and%20microbial%20dysbiosis%20in%20mice&rft.jtitle=Nature%20Communications&rft.date=2015&rft.volume=6&rft.spage=8141&rft.au=Huang,%20Yen-Lin&Chassard,%20Christophe&Hausmann,%20Martin&Von%20Itzstein,%20Mark&Hennet,%20Thierry&rft.genre=article&
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