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dc.contributor.authorMildenberger, Jennifer
dc.contributor.authorJohansson, Ida
dc.contributor.authorSergin, Ismail
dc.contributor.authorKjøbli, Eli
dc.contributor.authorDamås, Jan Kristian
dc.contributor.authorRazani, Babak
dc.contributor.authorFlo, Trude Helen
dc.contributor.authorBjørkøy, Geir
dc.date.accessioned2018-04-18T07:05:53Z
dc.date.available2018-04-18T07:05:53Z
dc.date.created2017-10-30T14:58:44Z
dc.date.issued2017
dc.identifier.citationAutophagy. 2017, 13 (10), 1664-1678.nb_NO
dc.identifier.issn1554-8627
dc.identifier.urihttp://hdl.handle.net/11250/2494562
dc.description.abstractInflammation is crucial in the defense against infections but must be tightly controlled to limit detrimental hyperactivation. Our diet influences inflammatory processes and omega-3 polyunsaturated fatty acids (n-3 PUFAs) have known anti-inflammatory effects. The balance of pro- and anti-inflammatory processes is coordinated by macrophages and macroautophagy/autophagy has recently emerged as a cellular process that dampens inflammation. Here we report that the n-3 PUFA docosahexaenoic acid (DHA) transiently induces cytosolic speckles of the autophagic receptor SQSTM1/p62 (sequestosome 1) (described as SQSTM1/p62-bodies) in macrophages. We suggest that the formation of SQSTM1/p62-bodies represents a fast mechanism of NFE2L2/Nrf2 (nuclear factor, erythroid 2 like 2) activation by recruitment of KEAP1 (kelch like ECH associated protein 1). Further, the autophagy receptor TAX1BP1 (Tax1 binding protein 1) and ubiquitin-editing enzyme TNFAIP3/A20 (TNF α induced protein 3) could be identified in DHA-induced SQSTM1/p62-bodies. Simultaneously, DHA strongly dampened the induction of pro-inflammatory genes including CXCL10 (C-X-C motif chemokine ligand 10) and we suggest that formation of SQSTM1/p62-bodies and activation of NFE2L2 leads to tolerance towards selective inflammatory stimuli. Finally, reduced CXCL10 levels were related to the improved clinical outcome in n-3 PUFA-supplemented heart-transplant patients and we propose CXCL10 as a robust marker for the clinical benefits mobilized by n-3 PUFA supplementation.nb_NO
dc.language.isoengnb_NO
dc.publisherTaylor & Francisnb_NO
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleN-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2nb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber1664-1678nb_NO
dc.source.volume13nb_NO
dc.source.journalAutophagynb_NO
dc.source.issue10nb_NO
dc.identifier.doi10.1080/15548627.2017.1345411
dc.identifier.cristin1508991
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.description.localcode© 2017 Jennifer Mildenberger, Ida Johansson, Ismail Sergin, Eli Kjøbli, Jan Kristian Dama s, Babak Razani, Trude Helen Flo, and Geir Bjørkøy. Published with license by Taylor & Francis This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.nb_NO
cristin.unitcode194,65,15,0
cristin.unitcode194,66,40,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.unitnameInstitutt for bioingeniørfag
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal