Evidence map›Paper›PMID 32038637›Full record

ArticleFrontiers in immunology2019

Sensory Ganglia-Specific TNF Expression Is Associated With Persistent Nociception After Resolution of Inflammation.

William Antonio Gonçalves, Barbara Maximino Rezende, Marcos Paulo Esteves de Oliveira, Lucas Secchim Ribeiro, Victor Fattori, Walison Nunes da Silva, Pedro Henrique Dias Moura Prazeres, Celso Martins Queiroz-Junior, Karina Talita de Oliveira Santana, Walyson Coelho Costa and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  12. Glioma Pericytes Promote Angiogenesis by Producing Periostin.Cellular and molecular neurobiology · 2022
    Review
  13. Article
  14. Sensory nerves in the spotlight of the stem cell niche.Stem cells translational medicine · 2021
    Review
  15. Acoustic Trauma Increases Ribbon Number and Size in Outer Hair Cells of the Mouse Cochlea.Journal of the Association for Research in Otolaryngology : JARO · 2021
    Article
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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

19 authors at 5 institutions in 3 countries.

William Antonio GonçalvesDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Barbara Maximino RezendeDepartamento de Enfermagem Básica, Escola de Enfermagem da Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Marcos Paulo Esteves de OliveiraDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Lucas Secchim RibeiroBiomediziniches Zentrum (BMZ), Institut für Angeborene Immunität, Rheinische Friedrich-Wilhelms-Universität Bonn, Venusberg, Germany.
Victor FattoriDepartamento de Patologia, Center of Biological Sciences, Londrina State University, Londrina, Brazil.
Walison Nunes da SilvaDepartamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Pedro Henrique Dias Moura PrazeresDepartamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Celso Martins Queiroz-JuniorDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Karina Talita de Oliveira SantanaDepartamento de Genética, Ecologia e Evolução, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Walyson Coelho CostaDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Vinícius Amorim BeltramiDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Vivian Vasconcelos CostaDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Alexander BirbrairDepartamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Waldiceu A VerriDepartamento de Patologia, Center of Biological Sciences, Londrina State University, Londrina, Brazil.
Fernando LopesInstitute of Parasitology and Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada.
Thiago Mattar CunhaDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, Brazil.
Mauro Martins TeixeiraDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Flávio Almeida AmaralDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Vanessa PinhoDepartamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Universidade Federal de Minas Gerais · BRUniversidade Estadual de Londrina · BRMcGill University · CAUniversidade de Ribeirão Preto · BRUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Joint pain is a distressing symptom of arthritis, and it is frequently persistent even after treatments which reduce local inflammation. Continuous production of algogenic factors activate/sensitize nociceptors in the joint structures and contribute to persistent pain, a challenging and difficult condition to treat. TNF is a crucial cytokine for the pathogenesis of several rheumatic diseases, and its inhibition is a mainstay of treatment to control joint symptoms, including pain. Here, we sought to investigate the inflammatory changes and the role of TNF in dorsal root ganglia (DRG) during persistent hypernociception after the resolution of acute joint inflammation. Using a model of antigen-induced arthritis, the peak of joint inflammation occurred 12-24 h after local antigen injection and was characterized by an intense influx of neutrophils, pro-inflammatory cytokine production, and joint damage. We found that inflammatory parameters in the joint returned to basal levels between 6 and 8 days after antigen-challenge, characterizing the resolving phase of joint inflammation. Mechanical hyperalgesia was persistent up to 14 days after joint insult. The persistent nociception was associated with the inflammatory status of DRG after cessation of acute joint inflammation. The late state of neuroinflammation in the ipsilateral side was evidenced by gene expression of TNF, TNFR2, IL-6, IL-1β, CXCL2, COX2, and iNOS in lumbar DRG (L3-L5) and leukocyte adhesion in the lumbar intumescent vessels between days 6 and 8. Moreover, there were signs of resident macrophage activation in DRG, as evidenced by an increase in Iba1-positive cells. Intrathecal or systemic injection of etanercept, an agent clinically utilized for TNF neutralization, at day 7 post arthritis induction, alleviated the persistent joint hyperalgesia by specific action in DRG. Our data suggest that neuroinflammation in DRG after the resolution of acute joint inflammation drives continuous neural sensitization resulting in persistent joint nociception in a TNF-dependent mechanism.

Indexed as

Gene ExpressionNociceptionAnimalsArthralgiaBiomarkersBiopsyDisease Models, AnimalDisease SusceptibilityGanglia, SpinalInflammationMaleMiceSpinal CordTumor Necrosis Factor-alphaBiomarkersTumor Necrosis Factor-alphaarthritisdorsal root ganglianeuroinflammationpainresolution of inflammationTNF

Identifiers

PMID32038637
PMCPMC6984351
OpenAlexW3002678256

What OpenQuestion holds

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Registered trials

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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.