Sensory neuron-associated macrophages as novel modulators of neuropathic pain

Autor(es)

Anibal Silva, Conceicao Elidianne ^{[1, 2]} ; Guimaraes, Rafaela Mano ^{[1, 2]} ; Cunha, Thiago Mattar ^{[3, 1, 4]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ctr Res Inflammatory Dis CRID, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Ribeira Preto Med Sch, Grad Programin Basic & Appl Immunol, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Sao Paulo - Brazil

^[4] Univ Sao Paulo Ribeira Preto, Dept Pharmacol Ribeirao Preto, Med Sch, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: PAIN REPORTS; v. 6, n. 1 2021.
• Citações Web of Science: 3

Resumo

The peripheral nervous system comprises an infinity of neural networks that act in the communication between the central nervous system and the most diverse tissues of the body. Along with the extension of the primary sensory neurons (axons and cell bodies), a population of resident macrophages has been described. These newly called sensory neuron-associated macrophages (sNAMs) seem to play an essential role in physiological and pathophysiological processes, including infection, autoimmunity, nerve degeneration/regeneration, and chronic neuropathic pain. After different types of peripheral nerve injury, there is an increase in the number and activation of sNAMs in the sciatic nerve and sensory ganglia. The activation of sNAMs and their participation in neuropathic pain development depends on the stimulation of pattern recognition receptors such as Toll-like receptors and Nod-like receptors, chemokines/cytokines, and microRNAs. On activation, sNAMs trigger the production of critical inflammatory mediators such as proinflammatory cytokines (eg, TNF and IL-1 beta) and reactive oxygen species that can act in the amplification of primary sensory neurons sensitization. On the other hand, there is evidence that sNAMs can produce antinociceptive mediators (eg, IL-10) that counteract neuropathic pain development. This review will present the cellular and molecular mechanisms behind the participation of sNAMs in peripheral nerve injury-induced neuropathic pain development. Understanding how sNAMs are activated and responding to nerve injury can help set novel targets for the control of neuropathic pain. (AU)

• Processo FAPESP: 20/05446-0 - Origem, dinâmica e perfil transcricional dos macrófagos dos gânglios sensitivos das raízes dorsais e nervo ciático em homestase e na dor neuropática
• Beneficiário: Conceição Elidianne Aníbal Silva
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• 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: 19/13829-0 - Papel da O-GlcNAcilação nas funções neuroinflamatórias dos astrócitos
• Beneficiário: Rafaela Mano Guimarães
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/50419-9 - Envolvimento dos canais iônicos TRPM2, HCN2 e do receptor AT2 em doenças inflamatórias
• Beneficiário: Thiago Mattar Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Regular