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dc.contributor.authorMC COY, CLAIREen
dc.contributor.authorO'NEILL, LUKE ANTHONY JOHNen
dc.contributor.authorDOYLE, SARAH LOUISEen
dc.date.accessioned2013-08-07T11:11:33Z
dc.date.available2013-08-07T11:11:33Z
dc.date.issued2013en
dc.date.submitted2013en
dc.identifier.citationDowling JK, McCoy CE, Doyle SL, Benlarbi N, Canavan M, O'Neill LA, Loscher CE, Conjugated linoleic acid suppresses IRF3 activation via modulation of CD14., The Journal of nutritional biochemistry, 24, 5, 2013, 920-928en
dc.identifier.otherYen
dc.identifier.urihttp://hdl.handle.net/2262/66888
dc.descriptionPUBLISHEDen
dc.description.abstractPolyunsaturated fatty acids (PUFA) can modulate the immune response, however the mechanism by which they exert this effect remains unclear. Previous studies have clearly demonstrated that the cis-9, trans-11 isomer of conjugated linoleic acid (c9,t11-CLA), found predominantly in beef and dairy products, can modulate the response of immune cells to the toll-like receptor (TLR) 4 ligand, lipopolysaccharide (LPS). This study aimed to investig ate further the mechanism by which these effects are mediated. Treatment of macrophages with c9,t11-CLA significantly decreased CD14 expression and partially blocked its association with lipid rafts following stimulation with LPS. Furthermore the c9,t11-CLA isomer inhibited both nuclear facto r- ? B (NF- ? B) and IRF3 activation following TLR4 ligation while eicosapentaenoic acid (EPA) only suppressed NF- ? B activation. Given that the ability of LPS to activate IRF3 downstream of TLR4 depends on internalisation of the TLR4 complex and involves CD14, we examined TLR4 endocytosis. Indeed the internalisation o f TLR4 to early endosomes following activation with LPS was markedly inhibited in c9,t11-CLA treated cells. These effects were not seen with the n-3 fat ty acid, EPA, which was used as a comparison. Our data demonstrates that c9,t11-CLA inhibits IRF3 activation via its effects on CD14 expression and localisation. This results in a decrease in the endocytosis of TLR4 which is necessary for IRF3 activation, revealing a novel mechanism by which this P UFA exerts its anti-inflammatory effects.en
dc.description.sponsorshipThis work was supported by funds from the Irish Research Council for Science, Engineering and Technology and Science Foundation Irelanden
dc.format.extent920-928en
dc.language.isoenen
dc.relation.ispartofseriesThe Journal of nutritional biochemistryen
dc.relation.ispartofseries24en
dc.relation.ispartofseries5en
dc.rightsYen
dc.subjectConjugated linoleic acid; IRF3; NFkappaB; CD14en
dc.subject.lcshConjugated linoleic acid; IRF3; NFkappaB; CD14en
dc.titleConjugated linoleic acid suppresses IRF3 activation via modulation of CD14.en
dc.typeJournal Articleen
dc.type.supercollectionscholarly_publicationsen
dc.type.supercollectionrefereed_publicationsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/laoneillen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/cmccoyen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/doyles8en
dc.identifier.rssinternalid84242en


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