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@ARTICLE{Gonalves:284085,
      author       = {Gonçalves, William Antonio and Rezende, Barbara Maximino
                      and Oliveira, Marcos Paulo Esteves de and Secchim Ribeiro,
                      Lucas and Fattori, Victor and Silva, Walison Nunes da and
                      Prazeres, Pedro Henrique Dias Moura and Queiroz-Junior,
                      Celso Martins and Santana, Karina Talita de Oliveira and
                      Costa, Walyson Coelho and Beltrami, Vinícius Amorim and
                      Costa, Vivian Vasconcelos and Birbrair, Alexander and Verri,
                      Waldiceu A. and Lopes, Fernando and Cunha, Thiago Mattar and
                      Teixeira, Mauro Martins and Amaral, Flávio Almeida and
                      Pinho, Vanessa},
      title        = {{S}ensory {G}anglia-{S}pecific {TNF} {E}xpression {I}s
                      {A}ssociated {W}ith {P}ersistent {N}ociception {A}fter
                      {R}esolution of {I}nflammation},
      journal      = {Frontiers in immunology},
      volume       = {10},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2026-00093},
      pages        = {3120},
      year         = {2020},
      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.},
      keywords     = {Animals / Arthralgia: etiology / Arthralgia: metabolism /
                      Arthralgia: pathology / Biomarkers / Biopsy / Disease
                      Models, Animal / Disease Susceptibility / Ganglia, Spinal:
                      metabolism / Gene Expression / Inflammation: etiology /
                      Inflammation: metabolism / Inflammation: pathology / Male /
                      Mice / Nociception / Spinal Cord / Tumor Necrosis
                      Factor-alpha: genetics / Tumor Necrosis Factor-alpha:
                      metabolism / TNF (Other) / arthritis (Other) / dorsal root
                      ganglia (Other) / neuroinflammation (Other) / pain (Other) /
                      resolution of inflammation (Other) / Biomarkers (NLM
                      Chemicals) / Tumor Necrosis Factor-alpha (NLM Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.3389/fimmu.2019.03120},
      url          = {https://pub.dzne.de/record/284085},
}