Evidence map›Paper›PMID 26868525›Full record

ArticleJournal of leukocyte biology2016

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

Izabela Galvão, Ana Carolina Fialho Dias, Livia Duarte Tavares, Irla Paula Stopa Rodrigues, Celso Martins Queiroz-Junior, Vivian Vasconcelos Costa, Alesandra Corte Reis, Rene Donizeti Ribeiro Oliveira, Paulo Louzada-Junior, Daniele Glória Souza and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Peripheral CD4Frontiers in immunology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Izabela GalvãoDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Ana Carolina Fialho DiasDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Livia Duarte TavaresDepartment of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Irla Paula Stopa RodriguesDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Celso Martins Queiroz-JuniorDepartment of Morphology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Vivian Vasconcelos CostaDepartment of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Alesandra Corte ReisDepartment of Morphology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Rene Donizeti Ribeiro OliveiraDivision of Rheumatology, School of Medicine of Ribeirao Preto, Universidade de São Paulo, Brazil.
Paulo Louzada-JuniorDivision of Rheumatology, School of Medicine of Ribeirao Preto, Universidade de São Paulo, Brazil.
Daniele Glória SouzaDepartment of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Lin LengDepartment of Medicine/Rheumatology, Yale University School of Medicine, The Anlyan Center, New Haven, Connecticut, USA.
Richard BucalaDepartment of Medicine/Rheumatology, Yale University School of Medicine, The Anlyan Center, New Haven, Connecticut, USA.
Lirlândia Pires SousaDepartment of Clinical Analysis and Toxicological, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Marcelo Torres BozzaLaboratory of Inflammation and Immunity, Department of Immunology, Institute of Microbiology, Universidade Federal do Rio de Janeiro, Brazil.
Mauro Martins TeixeiraDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil mmtex@icb.ufmg.br.
Flávio Almeida AmaralDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil famaral@icb.ufmg.br.
Universidade Federal de Minas Gerais · BRUniversidade de São Paulo · BRYale University · USUniversidade Federal do Rio de Janeiro · BR

Funding

Mechanisms of Rheumatoid Synovial Fibroblast ActivationR01AR049610 · NIAMS · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2002 to 2018
$5.0M
NIAMS NIH HHS R01 AR049610
6 · The paper itself

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.

Indexed as

Acute DiseaseAnimalsDisease Models, AnimalFemaleGoutHumansInflammationInjectionsInterleukin-1betaJointsMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMiddle AgedNeutrophilsReceptors, Interleukin-1Interleukin-1betaMacrophage Migration-Inhibitory FactorsReceptors, Interleukin-1Receptors, Interleukin-8AReceptors, Interleukin-8BRecombinant ProteinsRNA, MessengerUric AcidarthritischemokineinflammasomeMIF

Identifiers

PMID26868525
PMCPMC4952013
OpenAlexW2275520397

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.