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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/53841
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dc.creatorMarina Chaves de Oliveirapt_BR
dc.creatorLuciana Padua Tavarespt_BR
dc.creatorJuliana Priscila Vago da Silvapt_BR
dc.creatorNathália Vieira Batistapt_BR
dc.creatorCelso Martins Queiroz Juniorpt_BR
dc.creatorAngelica Thomaz Vieirapt_BR
dc.creatorGustavo Batista de Menezespt_BR
dc.creatorLirlândia Pires de Sousapt_BR
dc.creatorFons Van De Loopt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.creatorFlávio Almeida Amaralpt_BR
dc.creatorAdaliene Versiani Matos Ferreirapt_BR
dc.date.accessioned2023-05-23T21:05:38Z-
dc.date.available2023-05-23T21:05:38Z-
dc.date.issued2016-
dc.citation.volume11pt_BR
dc.citation.issue1pt_BR
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0146403pt_BR
dc.identifier.issn1932-6203pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/53841-
dc.description.resumoMetabolic alterations are associated with arthritis apart from obesity. However, it is still unclear which is the underlying process behind these metabolic changes. Here, we investigate the role of tumor necrosis factor (TNF) in this process in an acute model of antigen-induced arthritis (AIA). Immunized male BALB/c mice received an intra-articular injection of PBS (control) or methylated bovine serum albumin (mBSA) into their knees, and were also pre-treated with different drugs: Etanercept, an anti-TNF drug, DF2156A, a CXCR1/2 receptor antagonist, or a monoclonal antibody RB6-8C5 to deplete neutrophils. Local challenge with mBSA evoked an acute neutrophil influx into the knee joint, and enhanced the joint nociception, along with a transient systemic metabolic alteration (higher levels of glucose and lipids, and altered adipocytokines). Pre-treatment with the conventional biological Etanercept, an inhibitor of TNF action, ameliorated the nociception and the acute joint inflammation dominated by neutrophils, and markedly improved many of the altered systemic metabolites (glucose and lipids), adipocytokines and PTX3. However, the lessening of metabolic changes was not due to diminished accumulation of neutrophils in the joint by Etanercept. Reduction of neutrophil recruitment by pre-treating AIA mice with DF2156A, or even the depletion of these cells by using RB6-8C5 reduced all of the inflammatory parameters and hypernociception developed after AIA challenge, but could not prevent the metabolic changes. Therefore, the induction of joint inflammation provoked acute metabolic alterations which were involved with TNF. We suggest that the role of TNF in arthritis-associated metabolic changes is not due to local neutrophils, which are the major cells present in this model, but rather due to cytokines.pt_BR
dc.format.mimetypepdfpt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentENF - DEPARTAMENTO DE NUTRIÇÃOpt_BR
dc.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofPlos onept_BR
dc.rightsAcesso Abertopt_BR
dc.subjectTumor Necrosis Factorspt_BR
dc.subjectArthritispt_BR
dc.subjectNeutrophilspt_BR
dc.subject.otherFatores de Necrose Tumoralpt_BR
dc.subject.otherArtritept_BR
dc.subject.otherNeutrófilospt_BR
dc.titleTumor necrosis factor, but not neutrophils, alters the metabolic profile in acute experimental arthritispt_BR
dc.title.alternativeFator de necrose tumoral, mas não neutrófilos, altera o perfil metabólico na artrite experimental agudapt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146403#authcontribpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7423-9802pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5319-0210pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-8188-3738pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7884-7709pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4556-7671pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1042-9762pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5851-099Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6944-3008pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1695-0612pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2256-8652pt_BR
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