Sensory neuron-associated macrophages as novel modulators of neuropathic pain

Author(s)

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

Affiliation

^[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

• Document type: Review article
• Source: PAIN REPORTS; v. 6, n. 1 2021.
• Web of Science Citations: 3

Abstract

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)

• FAPESP's process: 20/05446-0 - Origin, dynamics and transcriptional profile of dorsal root ganglion and sciatic nerve macrophages in homeostasis and during neuropathic pain
• Grantee: Conceição Elidianne Aníbal Silva
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
• FAPESP's process: 19/13829-0 - Role of O-GlcNAcylation in the neuroinflammatory functions of astrocytes
• Grantee: Rafaela Mano Guimarães
• Support Opportunities: Scholarships in Brazil - Doctorate
• FAPESP's process: 17/50419-9 - Involvement of TRPM2, HCN2 ion channels and AT2 receptors in inflammatory diseases
• Grantee: Thiago Mattar Cunha
• Support Opportunities: Regular Research Grants