IL-27 Counteracts Neuropathic Pain Development Through Induction of IL-10

• Published in: Frontiers in immunology Vol. 10; p. 3059
• Main Authors: Fonseca, Miriam M, Davoli-Ferreira, Marcela, Santa-Cecília, Flávia, Guimarães, Rafaela M, Oliveira, Francisco F B, Kusuda, Ricardo, Ferreira, David W, Alves-Filho, José C, Cunha, Fernando Q, Cunha, Thiago M
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 28.01.2020
• Subjects: cytokines; glial cells; IL-10; IL-27; Immunology; macrophages; neuropathic pain; IL-27; glial cells; macrophages; neuropathic pain; cytokines; IL-10
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2019.03059

Neuroimmune-glia interactions have been implicated in the development of neuropathic pain. Interleukin-27 (IL-27) is a cytokine that presents regulatory activity in inflammatory conditions of the central nervous system. Thus, we hypothesized that IL-27 would participate in the neuropathic pain process. Here, we found that neuropathic pain caused by peripheral nerve injury (spared nerve injury model; SNI), was enhanced in IL-27-deficient mice, whereas nociceptive pain is similar to that of wild-type mice. SNI induced an increase in the expression of IL-27 and its receptor subunit ( ) in the sensory ganglia and spinal cord. IL-27 receptor was expressed mainly in resident macrophage, microglia, and astrocytes of the sensory ganglia and spinal cord, respectively. Finally, we identify that the antinociceptive effect of IL-27 was not observed in IL-10 mice. These results provided evidence that IL-27 is a cytokine produced after peripheral nerve injury that counteracts neuropathic pain development through induction of the antinociceptive cytokine IL-10. In summary, our study unraveled the role of IL-27 as a regulatory cytokine that counteracts the development of neuropathic pain after peripheral nerve damage. In conclusion, they indicate that immunotherapies based on IL-27 could emerge as possible therapeutic approaches for the prevention of neuropathic pain development after peripheral nerve injury.