Omega-3 fatty acids attenuate dendritic cell function via NF-κB independent of PPARγ.

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dc.contributor.author Draper, E en
dc.contributor.author Reynolds, Clare en
dc.contributor.author Canavan, M en
dc.contributor.author Mills, KH en
dc.contributor.author Loscher, CE en
dc.contributor.author Roche, HM en
dc.coverage.spatial United States en
dc.date.accessioned 2012-05-30T01:10:52Z en
dc.date.issued 2011-08 en
dc.identifier.citation Journal of Nutritional Biochemistry 22(8):784-790 Aug 2011 en
dc.identifier.uri http://hdl.handle.net/2292/18759 en
dc.description.abstract Long-chain n-3 polyunsaturated fatty acids (n-3 PUFA) have been shown to modulate the immune response and have therapeutic effects in inflammatory disorders. PUFA are also peroxisome proliferators-activator receptor-gamma (PPARγ) ligands; a family of ligand-activated transcription factors, which when activated antagonise the pro-inflammatory capability of nuclear factor κB (NF-κB). PPARγ plays a role in dendritic cell (DC) maturation and n-3 PUFA have been shown to affect DC maturation by decreasing activation of NF-κB. While n-3 PUFA can function as PPAR ligands, it is not known whether the NF-κB-mediated immunomodulatory properties of n-3 PUFA are PPARγ-dependent. In this study we examined whether the immunomodulatory effects of n-3 PUFA on DC activation were mediated through activation of PPARγ. Treatment of murine bone marrow derived DCs with docosahexaenoic acid (DHA; 25 μM) and eicosapentaenoic acid (EPA; 25 μM) attenuated LPS-induced DC maturation. This was characterised by suppression of IL-12 production and expression of CD40, CD80, CD86 and MHC II and enhanced production of IL-10 and expression of IL-10R. This was coincident with enhanced PPARγ expression, suppressed NF-κB activity and increased the physical interaction and cellular colocalization between NF-κB with PPARγ. To understand the functional implication of the physical association of PPARγ with NF-κB, we determined whether the specific PPARγ inhibitor, GW9662 could abolish the anti-inflammatory effect of n-3 PUFA Inhibiting PPARγ did not impede the NF-κB-mediated anti-inflammatory cytokine profile induced by EPA and DHA alone. Thus n-3 PUFA activate PPARγ and interact with NF-κB in DC. However, the anti-inflammatory effects of EPA and DHA on DCs are independent of PPARγ. en
dc.language eng en
dc.publisher Elsevier Inc. en
dc.relation.ispartofseries Journal of Nutritional Biochemistry en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.sherpa.ac.uk/romeo/issn/0955-2863/ en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.subject Animals en
dc.subject Anti-Inflammatory Agents en
dc.subject Blotting, Western en
dc.subject Bone Marrow Cells en
dc.subject Cell Differentiation en
dc.subject Cells, Cultured en
dc.subject Dendritic Cells en
dc.subject Docosahexaenoic Acids en
dc.subject Eicosapentaenoic Acid en
dc.subject Immunoprecipitation en
dc.subject Interleukin-10 en
dc.subject Interleukin-12 en
dc.subject Lipopolysaccharides en
dc.subject Mice en
dc.subject Mice, Inbred BALB C en
dc.subject NF-kappa B en
dc.subject PPAR gamma en
dc.title Omega-3 fatty acids attenuate dendritic cell function via NF-κB independent of PPARγ. en
dc.type Journal Article en
dc.identifier.doi 10.1016/j.jnutbio.2010.06.009 en
pubs.issue 8 en
pubs.begin-page 784 en
pubs.volume 22 en
dc.rights.holder Copyright: Elsevier Inc. en
dc.identifier.pmid 21111596 en
pubs.end-page 790 en
dc.rights.accessrights http://purl.org/eprint/accessRights/RestrictedAccess en
pubs.subtype Article en
pubs.elements-id 341390 en
pubs.org-id Liggins Institute en
dc.identifier.eissn 1873-4847 en
dc.identifier.pii S0955-2863(10)00167-1 en
pubs.record-created-at-source-date 2012-05-30 en
pubs.dimensions-id 21111596 en


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