CD36 Shunts Eicosanoid Metabolism to Repress CD14 Licensed Interleukin-1 beta Release and Inflammation

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dc.citation.volumev. 9
dc.contributor.authorZoccal, Karina F.
dc.contributor.authorGardinassi, Luiz G.
dc.contributor.authorSorgi, Carlos A.
dc.contributor.authorMeirelles, Alyne F. G.
dc.contributor.authorBordon, Karla C. F.
dc.contributor.authorGlezer, Isaias [UNIFESP]
dc.contributor.authorCupo, Palmira
dc.contributor.authorMatsuno, Alessandra K.
dc.contributor.authorBollela, Valdes R.
dc.contributor.authorArantes, Eliane C.
dc.contributor.authorGuimaraes, Francisco S.
dc.contributor.authorFaccioli, Lucia Helena
dc.coverageLausanne
dc.date.accessioned2020-07-20T16:30:59Z
dc.date.available2020-07-20T16:30:59Z
dc.date.issued2018
dc.description.abstractInterleukin (IL)-1 beta is a potential target for treatment of several inflammatory diseases, including envenomation by the scorpion Tityus serrulatus. In this context, bioactive lipids such as prostaglandin (PG)E-2 and leukotriene (LT)B-4 modulate the production of IL-1 beta by innate immune cells. Pattern recognition receptors (PRRs) that perceive T. serrulatus venom (TsV), and orchestrate LTB4, PGE(2), and cyclic adenosine monophosphate (cAMP) production to regulate IL-1 beta release are unknown. Furthermore, molecular mechanisms driving human cell responses to TsV remain uncharacterized. Here, we identified that both CD14 and CD36 control the synthesis of bioactive lipids, inflammatory cytokines, and mortality mediated by TsV. CD14 induces PGE(2)/cAMP/IL-1 beta release and inflammation. By contrast, CD36 shunts eicosanoid metabolism toward production of LTB4, which represses the PGE(2)/cAMP/IL-1 beta axis and mortality. Of importance, the molecular mechanisms observed in mice strongly correlate with those of human cell responses to TsV. Overall, this study provides major insights into molecular mechanisms connecting CD14 and CD36 with differential eicosanoid metabolism and inflammation mediated by IL-1 beta.en
dc.description.affiliationUniv Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, Ribeirao Preto, Brazil
dc.description.affiliationUniv Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Fis & Quim, Ribeirao Preto, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Bioquim, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Fac Med Ribeirao Preto, Dept Puericultura & Pediat, Ribeirao Preto, Brazil
dc.description.affiliationUniv Sao Paulo, Fac Med Ribeirao Preto, Dept Clin Med, Ribeirao Preto, Brazil
dc.description.affiliationUniv Sao Paulo, Fac Med Ribeirao Preto, Dept Farmacol, Ribeirao Preto, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Bioquim, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
dc.description.sponsorshipCEPID Redoxoma (FAPESP)
dc.description.sponsorshipIDFAPESP: 2014/07125-6
dc.description.sponsorshipIDFAPESP: 2015/00658-1
dc.description.sponsorshipIDFAPESP: 2014/03332-7
dc.description.sponsorshipIDCEPID-FAPESP: 2013/07937-8
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.3389/fimmu.2018.00890
dc.identifier.citationFrontiers In Immunology. Lausanne, v. 9, p. -, 2018.
dc.identifier.doi10.3389/fimmu.2018.00890
dc.identifier.fileWOS000431027200001.pdf
dc.identifier.issn1664-3224
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55627
dc.identifier.wosWOS:000431027200001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Immunology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectinterleukin-1 betaen
dc.subjectleukotriene B-4en
dc.subjectprostaglandin E-2en
dc.subjectcyclic adenosine monophosphateen
dc.subjectCD36 receptoren
dc.subjectCD14 receptoren
dc.subjectvenomen
dc.titleCD36 Shunts Eicosanoid Metabolism to Repress CD14 Licensed Interleukin-1 beta Release and Inflammationen
dc.typeinfo:eu-repo/semantics/article
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