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dc.contributor.author
Becker, Eugenia
dc.contributor.author
Bengs, Susan
dc.contributor.author
Aluri, Sirisha
dc.contributor.author
Opitz, Lennart
dc.contributor.author
Atrott, Kirstin
dc.contributor.author
Stanzel, Claudia
dc.contributor.author
Ruiz Castro, Pedro A.
dc.contributor.author
Rogler, Gerhard
dc.contributor.author
Frey-Wagner, Isabelle
dc.date.accessioned
2018-01-30T12:25:17Z
dc.date.available
2018-01-18T14:06:50Z
dc.date.available
2018-01-30T12:25:17Z
dc.date.issued
2016-11-17
dc.identifier.other
10.1038/srep37082
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/230896
dc.identifier.doi
10.3929/ethz-b-000230896
dc.description.abstract
Inflammatory bowel disease (IBD) may develop due to an inflammatory response to commensal gut microbiota triggered by environmental factors in a genetically susceptible host. Isotretinoin (acne therapy) has been inconsistently associated with IBD onset and flares but prior treatment with antibiotics, also associated with IBD development, complicates the confirmation of this association. Here we studied in mice whether doxycycline, metronidazole or isotretinoin induce epigenetic modifications, and consequently change T-cell mRNA expression and/or function directly after treatment and after a 4 week recovery period. Isotretinoin induced IL-10 signaling in Tregs and naive T-cells directly after treatment and reduced effector T-cell proliferation alone and in co-culture with Tregs. Metronidazole activated processes associated with anti-inflammatory pathways in both T-cell subsets directly after the treatment period whereas doxycycline induced an immediate pro-inflammatory expression profile that resolved after the recovery period. Long-term changes indicated an inhibition of proliferation by doxycycline and induction of beneficial immune and metabolic pathways by metronidazole. Persistent alterations in microRNA and mRNA expression profiles after the recovery period indicate that all three medications may induce long-term epigenetic modifications in both T-cell subsets. Yet, our data do not support the induction of a long-term pro-inflammatory phenotype in murine Tregs and naive T-cells.
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.subject
Immunogenetics
en_US
dc.subject
Immunological memory
en_US
dc.subject
Imprinting
en_US
dc.subject
Inflammatory bowel disease
en_US
dc.title
Doxycycline, metronidazole and isotretinoin: Do they modify microRNA/mRNA expression profiles and function in murine T-cells?
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
ethz.journal.title
Scientific Reports
ethz.journal.volume
6
en_US
ethz.journal.issue
1
en_US
ethz.pages.start
37082
en_US
ethz.size
16 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.publication.place
S.l.
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00003 - Schulleitung und Dienste::00022 - Bereich VP Forschung & Wirtschaftsbez. / Domain VP Research & Corporate Relations::02207 - Functional Genomics Center Zürich / Functional Genomics Center Zürich
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00003 - Schulleitung und Dienste::00022 - Bereich VP Forschung & Wirtschaftsbez. / Domain VP Research & Corporate Relations::02207 - Functional Genomics Center Zürich / Functional Genomics Center Zürich
ethz.date.deposited
2018-01-18T14:06:50Z
ethz.source
BATCH
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2018-01-30T12:25:24Z
ethz.rosetta.lastUpdated
2019-01-02T11:30:30Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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