Macrophage inflammatory state in Type 1 diabetes: triggered by NLRP3/iNOS pathway and attenuated by docosahexaenoic acid

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dc.contributorDiretoria Técnicapt_BR
dc.contributor.authorDavanso, Mariana Rodriguespt_BR
dc.contributor.authorCrisma, Amanda Rabellopt_BR
dc.contributor.authorBraga, Tárcio Teodoropt_BR
dc.contributor.authorMasi, Laureane Nunespt_BR
dc.contributor.authorAmaral, Cátia Lira dopt_BR
dc.contributor.authorLeal, Vinícius Nunes Cordeiropt_BR
dc.contributor.authorLima, Dhêmerson Souza dept_BR
dc.contributor.authorPatente, Thiago Andradept_BR
dc.contributor.authorBarbuto, José Alexandrept_BR
dc.contributor.authorCorrêa-Giannella, Maria L.pt_BR
dc.contributor.authorLauterbach, Mariopt_BR
dc.contributor.authorKolbe, Carl Christianpt_BR
dc.contributor.authorLatz, Eickept_BR
dc.contributor.authorCamara, Niels Olsen Saraivapt_BR
dc.contributor.authorPontillo, Alessandrapt_BR
dc.contributor.authorCuri, Ruipt_BR
dc.identifier.citationDavanso MR, Crisma AR, Braga TT, Masi LN, Amaral CL, Leal VNC, et al. Macrophage inflammatory state in Type 1 diabetes: triggered by NLRP3/iNOS pathway and attenuated by docosahexaenoic acid. Clin. Sci.. 2021 Jan;135(1):19-34. doi:10.1042/CS20201348.pt_BR
dc.description.abstractType 1 diabetes mellitus (T1D) is a chronic autoimmune disease characterized by insulin-producing pancreatic β-cell destruction and hyperglycemia. While monocytes and NOD-like receptor family-pyrin domain containing 3 (NLRP3) are associated with T1D onset and development, the specific receptors and factors involved in NLRP3 inflammasome activation remain unknown. Herein, we evaluated the inflammatory state of resident peritoneal macrophages (PMs) from genetically modified non-obese diabetic (NOD), NLRP3-KO, wild-type (WT) mice and in peripheral blood mononuclear cells (PBMCs) from human T1D patients. We also assessed the effect of docosahexaenoic acid (DHA) on the inflammatory status. Macrophages from STZ-induced T1D mice exhibited increased inflammatory cytokine/chemokine levels, nitric oxide (NO) secretion, NLRP3 and iNOS protein levels, and augmented glycolytic activity compared to control animals. In PMs from NOD and STZ-induced T1D mice, DHA reduced NO production and attenuated the inflammatory state. Furthermore, iNOS and IL-1β protein expression levels and NO production were lower in the PMs from diabetic NLRP3-KO mice than from WT mice. We also observed increased IL-1β secretion in PBMCs from T1D patients and immortalized murine macrophages treated with advanced glycation end products and palmitic acid. The present study demonstrated that the resident PMs are in a proinflammatory state characterized by increased NLRP3/iNOS pathway-mediated NO production, up-regulated proinflammatory cytokine/chemokine receptor expression and altered glycolytic activity. Notably, ex vivo treatment with DHA reverted the diabetes-induced changes and attenuated the macrophage inflammatory state. It is plausible that DHA supplementation could be employed as adjuvant therapy for treating individuals with T1D.pt_BR
dc.description.sponsorship(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.description.sponsorship(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorship(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.relation.ispartofClinical Sciencept_BR
dc.rightsRestricted accesspt_BR
dc.titleMacrophage inflammatory state in Type 1 diabetes: triggered by NLRP3/iNOS pathway and attenuated by docosahexaenoic acidpt_BR
dc.contributor.external(USP) Universidade de São Paulopt_BR
dc.contributor.externalUniversity of Bonnpt_BR
dc.contributor.external(UFPR) Universidade Federal do Paranápt_BR
dc.contributor.external(UNICSUL) Universidade Cruzeiro do Sulpt_BR
dc.contributor.external(UEG) Universidade Estadual de Goiáspt_BR
dc.contributor.external(UNINOVE) Universidade Nove de Julhopt_BR
dc.subject.keywordomega-3 fatty acidspt_BR
dc.subject.keywordtype 1 diabetespt_BR
dc.relation.ispartofabbreviatedClin Scipt_BR
dc.identifier.citationabntv. 135, n. 1, p. 19-34, jan. 2021pt_BR
dc.identifier.citationvancouver2021 Jan;135(1):19-34pt_BR
dc.contributor.butantanCuri, Rui|:Diretor|:Diretoria Técnicapt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦pt_BR
dc.sponsorship.butantan(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico¦¦161731/2012-0pt_BR
dc.sponsorship.butantan(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
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