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Tytuł pozycji:

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

Tytuł:
Sensory Ganglia-Specific TNF Expression Is Associated With Persistent Nociception After Resolution of Inflammation.
Autorzy:
Gonçalves WA; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Rezende BM; Departamento de Enfermagem Básica, Escola de Enfermagem da Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
de Oliveira MPE; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Ribeiro LS; Biomediziniches Zentrum (BMZ), Institut für Angeborene Immunität, Rheinische Friedrich-Wilhelms-Universität Bonn, Venusberg, Germany.
Fattori V; Departamento de Patologia, Center of Biological Sciences, Londrina State University, Londrina, Brazil.
da Silva WN; Departamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Prazeres PHDM; Departamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Queiroz-Junior CM; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Santana KTO; Departamento de Genética, Ecologia e Evolução, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Costa WC; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Beltrami VA; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Costa VV; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Birbrair A; Departamento de Patologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Verri WA Jr; Departamento de Patologia, Center of Biological Sciences, Londrina State University, Londrina, Brazil.
Lopes F; Institute of Parasitology and Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada.
Cunha TM; Departamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, Brazil.
Teixeira MM; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Amaral FA; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Pinho V; Departamento de Morfologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Źródło:
Frontiers in immunology [Front Immunol] 2020 Jan 20; Vol. 10, pp. 3120. Date of Electronic Publication: 2020 Jan 20 (Print Publication: 2019).
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: [Lausanne : Frontiers Research Foundation]
MeSH Terms:
Gene Expression*
Nociception*
Ganglia, Spinal/*metabolism
Tumor Necrosis Factor-alpha/*genetics
Animals ; Arthralgia/etiology ; Arthralgia/metabolism ; Arthralgia/pathology ; Biomarkers ; Biopsy ; Disease Models, Animal ; Disease Susceptibility ; Inflammation/etiology ; Inflammation/metabolism ; Inflammation/pathology ; Male ; Mice ; Spinal Cord ; Tumor Necrosis Factor-alpha/metabolism
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Contributed Indexing:
Keywords: TNF; arthritis; dorsal root ganglia; neuroinflammation; pain; resolution of inflammation
Substance Nomenclature:
0 (Biomarkers)
0 (Tumor Necrosis Factor-alpha)
Entry Date(s):
Date Created: 20200211 Date Completed: 20201116 Latest Revision: 20201116
Update Code:
20240105
PubMed Central ID:
PMC6984351
DOI:
10.3389/fimmu.2019.03120
PMID:
32038637
Czasopismo naukowe
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.
(Copyright © 2020 Gonçalves, Rezende, Oliveira, Ribeiro, Fattori, Silva, Prazeres, Queiroz-Junior, Santana, Costa, Beltrami, Costa, Birbrair, Verri, Lopes, Cunha, Teixeira, Amaral and Pinho.)

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