The NOD2 signaling in peripheral macrophages contributes to neuropathic pain development

Autor(es):Mostrar menos -

Santa-Cecilia, V, Flavia ; Ferreira, David W. ^[1] ; Guimaraes, Rafaela M. ^[1] ; Cecilio, Nerry T. ^[1] ; Fonseca, Miriam M. ^[1] ; Lopes, Alexandre H. ^[1] ; Davoli-Ferreira, Marcela ^[1] ; Kusuda, Ricardo ^[1] ; Souza, Guilherme R. ^[1] ; Nachbur, Ueli ^{[2, 3]} ; Alves-Filho, Jose C. ^[1] ; Teixeira, Mauro M. ^[4] ; Zamboni, Dario S. ^[5] ; Cunha, Fernando Q. ^[1] ; Cunha, Thiago M. ^[1]

Afiliação do(s) autor(es)

^[1] Santa-Cecilia, Flavia, V, Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, CRID, Ribeirao Preto, SP - Brazil

^[2] Walter & Eliza Hall Inst Med Res, Parkville, Vic - Australia

^[3] Univ Melbourne, Dept Med Biol, Melbourne, Vic - Australia

^[4] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Lab Imunofarmacol, Belo Horizonte, MG - Brazil

^[5] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Cellular Biol, Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Pain; v. 160, n. 1, p. 102-116, JAN 2019.
• Citações Web of Science: 4

Resumo

Neuropathic pain is one of the most important types of chronic pain. It is caused by neuronal damage. Clinical and experimental studies suggest a critical role for neuroimmune interactions in the development of neuropathic pain. In this article, we have shown that the cytoplasmic receptor Nod-like receptor-2, NOD2, and its adaptor-signaling molecule RIPK2 participate in the development of neuropathic pain after peripheral nerve injury (spared nerve injury model). The activation of NOD2 signaling in peripheral macrophage mediates the development of neuropathic pain through the production of pronociceptive cytokines (tumor necrosis factor and IL-1 beta). This study found that peripheral nerve injury promoted a systemic increase in the NOD2 ligand. These results highlight a previously undetermined role for NOD2 signaling in the development of neuropathic pain, suggesting a new potential target for preventing neuropathic pain. (AU)

• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Temático