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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The NOD2 signaling in peripheral macrophages contributes to neuropathic pain development

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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]
Total Authors: 15
[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
Total Affiliations: 5
Document type: Journal article
Source: Pain; v. 160, n. 1, p. 102-116, JAN 2019.
Web of Science Citations: 1

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)

FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
Grantee:Fernando de Queiroz Cunha
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis
Grantee:Fernando de Queiroz Cunha
Support type: Research Projects - Thematic Grants