Autor: |
Miriam M. Fonseca, Marcela Davoli-Ferreira, Flávia Santa-Cecília, Rafaela M. Guimarães, Francisco F. B. Oliveira, Ricardo Kusuda, David W. Ferreira, José C. Alves-Filho, Fernando Q. Cunha, Thiago M. Cunha |
Jazyk: |
angličtina |
Rok vydání: |
2020 |
Předmět: |
|
Zdroj: |
Frontiers in Immunology, Vol 10 (2020) |
Druh dokumentu: |
article |
ISSN: |
1664-3224 |
DOI: |
10.3389/fimmu.2019.03059 |
Popis: |
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 (Wsx1) 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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
|