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Gout: HELP
Articles by Vivian Vasconcelos Costa
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Vivian V. Costa wrote the following 5 articles about Gout.
 
+ Citations + Abstracts
1 Article Phosphoinositide-3 kinase gamma regulates caspase-1 activation and leukocyte recruitment in acute murine gout. 2019

Tavares, Lívia D / Galvão, Izabela / Costa, Vivian V / Batista, Nathalia V / Rossi, Lívia C R / Brito, Camila B / Reis, Alesandra C / Queiroz-Junior, Celso M / Braga, Amanda D / Coelho, Fernanda M / Dias, Ana C / Zamboni, Dario S / Pinho, Vanessa / Teixeira, Mauro M / Amaral, Flávio A / Souza, Daniele G. ·Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Vollum Institute, Oregon Health and Science University, Portland, Oregon, USA. · Department of Cell Biology, Medical School of Ribeirão Preto, University of São Paulo FMRP/USP, Ribeirão Preto, São Paulo, Brazil. ·J Leukoc Biol · Pubmed #31392775.

ABSTRACT: This study investigates the participation of PI3Kγ in the development of joint inflammation and dysfunction in an experimental model of acute gout in mice. Acute gout was induced by injection of monosodium urate (MSU) crystals into the tibiofemoral joint of mice. The involvement of PI3Kγ was evaluated using a selective inhibitor and mice deficient for PI3Kγ (PI3Kγ

2 Article Annexin A1 promotes timely resolution of inflammation in murine gout. 2017

Galvão, Izabela / Vago, Juliana P / Barroso, Livia C / Tavares, Luciana P / Queiroz-Junior, Celso M / Costa, Vivian V / Carneiro, Fernanda S / Ferreira, Tatiana P / Silva, Patricia M R / Amaral, Flávio A / Sousa, Lirlândia P / Teixeira, Mauro M. ·Imunofarmacologia, Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. · Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. · Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. · Laboratório de Inflamação, Instituto Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil. ·Eur J Immunol · Pubmed #27995621.

ABSTRACT: Gout is a self-limited inflammatory disease caused by deposition of monosodium urate (MSU) crystals in the joints. Resolution of inflammation is an active process leading to restoration of tissue homeostasis. Here, we studied the role of Annexin A1 (AnxA1), a glucocorticoid-regulated protein that has anti-inflammatory and proresolving actions, in resolution of acute gouty inflammation. Injection of MSU crystals in the knee joint of mice induced inflammation that was associated with expression of AnxA1 during the resolving phase of inflammation. Neutralization of AnxA1 with antiserum or blockade of its receptor with BOC-1 (nonselective) or WRW

3 Article Macrophage migration inhibitory factor drives neutrophil accumulation by facilitating IL-1β production in a murine model of acute gout. 2016

Galvão, Izabela / Dias, Ana Carolina Fialho / Tavares, Livia Duarte / Rodrigues, Irla Paula Stopa / Queiroz-Junior, Celso Martins / Costa, Vivian Vasconcelos / Reis, Alesandra Corte / Ribeiro Oliveira, Rene Donizeti / Louzada-Junior, Paulo / Souza, Daniele Glória / Leng, Lin / Bucala, Richard / Sousa, Lirlândia Pires / Bozza, Marcelo Torres / Teixeira, Mauro Martins / Amaral, Flávio Almeida. ·Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Department of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Department of Morphology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Division of Rheumatology, School of Medicine of Ribeirao Preto, Universidade de São Paulo, Brazil. · Department of Medicine/Rheumatology, Yale University School of Medicine, The Anlyan Center, New Haven, Connecticut, USA. · Department of Clinical Analysis and Toxicological, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. · Laboratory of Inflammation and Immunity, Department of Immunology, Institute of Microbiology, Universidade Federal do Rio de Janeiro, Brazil. · Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil mmtex@icb.ufmg.br. · Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil famaral@icb.ufmg.br. ·J Leukoc Biol · Pubmed #26868525.

ABSTRACT: This study evaluated the role of macrophage migration inhibitory factor in inflammation caused by monosodium urate crystals. The concentration of macrophage migration inhibitory factor was increased in synovial fluid of patients with acute gout, and there was a positive correlation between intra-articular macrophage migration inhibitory factor and IL-1β concentrations. In mice, the injection of monosodium urate crystals into the knee joint increased the levels of macrophage migration inhibitory factor in macrophages and in inflamed tissue. The injection of recombinant macrophage migration inhibitory factor into the joint of mice reproduced the inflammatory response observed in acute gout, including histologic changes, the recruitment of neutrophils, and increased levels of IL-1β and CXCL1. Importantly, the accumulation of neutrophils and the amount IL-1β in the joints were reduced in macrophage migration inhibitory factor-deficient mice when injected with monosodium urate crystals. We observed a similar effect when we blocked macrophage migration inhibitory factor with (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid or anti-macrophage migration inhibitory factor. In addition, the blockade of IL-1R and CXCR2 reduced recombinant macrophage migration inhibitory factor-induced neutrophil recruitment. Mechanistically, recombinant macrophage migration inhibitory factor is important for the synthesis of il1β mRNA in vivo and in isolated macrophages. Altogether, macrophage migration inhibitory factor promotes neutrophil accumulation and is important for IL-1β production, which are 2 crucial events contributing to the pathogenesis of acute gout.

4 Article Transmembrane TNF-α is sufficient for articular inflammation and hypernociception in a mouse model of gout. 2016

Amaral, Flávio A / Bastos, Leandro F S / Oliveira, Thiago H C / Dias, Ana C F / Oliveira, Vívian L S / Tavares, Lívia D / Costa, Vivian V / Galvão, Izabela / Soriani, Frederico M / Szymkowski, David E / Ryffel, Bernhard / Souza, Danielle G / Teixeira, Mauro M. ·Immunopharmacology Lab, Department of Biochemistry and Immunology, Federal University of Minas, Gerais, Brazil. · Department of Microbiology, Federal University of Minas, Gerais, Brazil. · Department of General Biology, Federal University of Minas, Gerais, Brazil. · Xencor, Monrovia, USA. · Molecular Immunology and Embryology, Centre National de la Recherche Scientifique, Orléans, France. ·Eur J Immunol · Pubmed #26449770.

ABSTRACT: Gout manifests as recurrent episodes of acute joint inflammation and pain due to the deposition of monosodium urate (MSU) crystals within the affected tissue in a process dependent on NLRP3 inflammasome activation. The synthesis, activation, and release of IL-1β are crucial for MSU-induced inflammation. The current study evaluated the mechanism by which TNF-α contributed to MSU-induced inflammation. Male C57BL/6J or transgenic mice were used in this study and inflammation was induced by the injection of MSU crystals into the joint. TNF-α was markedly increased in the joint after the injection of MSU. There was inhibition in the infiltration of neutrophils, production of CXCL1 and IL-1β, and decreased hypernociception in mice deficient for TNF-α or its receptors. Pharmacological blockade of TNF-α with Etanercept or pentoxyfylline produced similar results. Mechanistically, TNF-α blockade resulted in lower amounts of IL-1β protein and pro-IL-1β mRNA transcripts in joints. Gene-modified mice that express only transmembrane TNF-α had an inflammatory response similar to that of WT mice and blockade of soluble TNF-α (XPro™1595) did not decrease MSU-induced inflammation. In conclusion, TNF-α drives expression of pro-IL-1β mRNA and IL-1β protein in experimental gout and that its transmembrane form is sufficient to trigger MSU-induced inflammation in mice.

5 Article NLRP3 inflammasome-mediated neutrophil recruitment and hypernociception depend on leukotriene B(4) in a murine model of gout. 2012

Amaral, Flávio A / Costa, Vivian V / Tavares, Livia D / Sachs, Daniela / Coelho, Fernanda M / Fagundes, Caio T / Soriani, Frederico M / Silveira, Tatiana N / Cunha, Larissa D / Zamboni, Dario S / Quesniaux, Valerie / Peres, Raphael S / Cunha, Thiago M / Cunha, Fernando Q / Ryffel, Bernhard / Souza, Daniele G / Teixeira, Mauro M. ·Universidade Federal de Minas Gerais, Minas Gerais, Brazil. ·Arthritis Rheum · Pubmed #21952942.

ABSTRACT: OBJECTIVE: Deposition of monosodium urate monohydrate (MSU) crystals in the joints promotes an intense inflammatory response and joint dysfunction. This study evaluated the role of the NLRP3 inflammasome and 5-lipoxygenase (5-LOX)-derived leukotriene B(4) (LTB(4) ) in driving tissue inflammation and hypernociception in a murine model of gout. METHODS: Gout was induced by injecting MSU crystals into the joints of mice. Wild-type mice and mice deficient in NLRP3, ASC, caspase 1, interleukin-1β (IL-1β), IL-1 receptor type I (IL-1RI), IL-18R, myeloid differentiation factor 88 (MyD88), or 5-LOX were used. Evaluations were performed to assess neutrophil influx, LTB(4) activity, cytokine (IL-1β, CXCL1) production (by enzyme-linked immunosorbent assay), synovial microvasculature cell adhesion (by intravital microscopy), and hypernociception. Cleaved caspase 1 and production of reactive oxygen species (ROS) were analyzed in macrophages by Western blotting and fluorometric assay, respectively. RESULTS: Injection of MSU crystals into the knee joints of mice induced neutrophil influx and neutrophil-dependent hypernociception. MSU crystal-induced neutrophil influx was CXCR2-dependent and relied on the induction of CXCL1 in an NLRP3/ASC/caspase 1/IL-1β/MyD88-dependent manner. LTB(4) was produced rapidly after injection of MSU crystals, and this was necessary for caspase 1-dependent IL-1β production and consequent release of CXCR2-acting chemokines in vivo. In vitro, macrophages produced LTB(4) after MSU crystal injection, and LTB(4) was relevant in the MSU crystal-induced maturation of IL-1β. Mechanistically, LTB(4) drove MSU crystal-induced production of ROS and ROS-dependent activation of the NLRP3 inflammasome. CONCLUSION: These results reveal the role of the NLRP3 inflammasome in mediating MSU crystal-induced inflammation and dysfunction of the joints, and highlight a previously unrecognized role of LTB(4) in driving NLRP3 inflammasome activation in response to MSU crystals, both in vitro and in vivo.