• Pain · Jan 2019

    The NOD2 signaling in peripheral macrophages contributes to neuropathic pain development.

    • Flávia V Santa-Cecília, David W Ferreira, Rafaela M Guimaraes, Nerry T Cecilio, Miriam M Fonseca, Alexandre H Lopes, Marcela Davoli-Ferreira, Ricardo Kusuda, Guilherme R Souza, Ueli Nachbur, José C Alves-Filho, Mauro M Teixeira, Dario S Zamboni, Fernando Q Cunha, and Thiago M Cunha.
    • Center for Research in Inflammatory Diseases (CRID), Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
    • Pain. 2019 Jan 1; 160 (1): 102-116.

    AbstractNeuropathic 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-1β). 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.

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