Palmitoleic acid reduces the inflammation in LPS-stimulated macrophages by inhibition of NF kappa B, independently of PPARs

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dc.contributor.authorSouza, Camila O.
dc.contributor.authorTeixeira, Alexandre A. S.
dc.contributor.authorBiondo, Luana A.
dc.contributor.authorSilveira, Loreana S. [UNESP]
dc.contributor.authorCalder, Philip C.
dc.contributor.authorRosa Neto, Jose C.
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniv Southampton
dc.date.accessioned2018-11-26T17:29:44Z
dc.date.available2018-11-26T17:29:44Z
dc.date.issued2017-05-01
dc.description.abstractPalmitoleic acid (PM, 16:1n-7) has anti-inflammatory properties that could be linked to higher expression of PPAR, an inhibitor of NFB. Macrophages play a major role in the pathogenesis of chronic inflammation, however, the effects of PM on macrophages are underexplored. Thus, we aimed to investigate the effects of PM in activated macrophages as well the role of PPAR. Primary macrophages were isolated from C57BL/6 wild type (WT) and PPAR knockout (KO) mice, cultured under standard conditions and exposed to lipopolysaccharides LPS (2.5g/ml) and PM 600mol/L conjugated with albumin for 24hours. The stimulation with LPS increased the production of interleukin (IL)-6 and IL-1 while PM decreased the production of IL-6 in WT macrophages. In KO macrophages, LPS increased the production of tumour necrosis factor (TNF)- and IL-6 and PM decreased the production of TNF. The expression of inflammatory markers such NFB and IL1 were increased by LPS and decreased by PM in both WT and KO macrophages. PM reduced the expression of MyD88 and caspase-1 in KO macrophages, and the expression of TLR4 and HIF-1 in both WT and KO macrophages, although LPS had no effect. CD86, an inflammatory macrophage marker, was reduced by PM independently of genotype. PM increased PPAR and reduced PPAR gene expression in macrophages of both genotypes, and increased ACOX-1 expression in KO macrophages. In conclusion, PM promotes anti-inflammatory effects in macrophages exposed to LPS through inhibition of inflammasome pathway, which was independent of PPAR, PPAR? and AMPK, thus the molecular mechanisms of anti-inflammatory response caused by PM is still unclear.en
dc.description.affiliationUniv Sao Paulo, Dept Cell & Dev Biol, Sao Paulo, Brazil
dc.description.affiliationState Univ Sao Paulo, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, Brazil
dc.description.affiliationUniv Southampton, Human Dev & Hlth, Southampton, Hants, England
dc.description.affiliationUnespState Univ Sao Paulo, Exercise & Immunometab Res Grp, Dept Phys Educ, Presidente Prudente, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 2013/04765-1
dc.description.sponsorshipIdFAPESP: 2016/01409-8
dc.format.extent566-575
dc.identifierhttp://dx.doi.org/10.1111/1440-1681.12736
dc.identifier.citationClinical And Experimental Pharmacology And Physiology. Hoboken: Wiley, v. 44, n. 5, p. 566-575, 2017.
dc.identifier.doi10.1111/1440-1681.12736
dc.identifier.issn1440-1681
dc.identifier.urihttp://hdl.handle.net/11449/162739
dc.identifier.wosWOS:000399902200005
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofClinical And Experimental Pharmacology And Physiology
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectimmune cell
dc.subjectinflammasome complex
dc.subjectmacrophage
dc.subjectmonounsaturated fatty acid
dc.subjectpalmitoleate
dc.subjectPPAR knockout mice
dc.titlePalmitoleic acid reduces the inflammation in LPS-stimulated macrophages by inhibition of NF kappa B, independently of PPARsen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderWiley-Blackwell

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