| Texto completo | |
| Autor(es): |
Fonseca, Miriam M.
;
Davoli-Ferreira, Marcela
;
Santa-Cecilia, Flavia
;
Guimaraes, Rafaela M.
;
Oliveira, Francisco F. B.
;
Kusuda, Ricardo
;
Ferreira, David W.
;
Alves-Filho, Jose C.
;
Cunha, Fernando Q.
;
Cunha, Thiago M.
Número total de Autores: 10
|
| Tipo de documento: | Artigo Científico |
| Fonte: | FRONTIERS IN IMMUNOLOGY; v. 10, p. 14-pg., 2020-01-28. |
| Resumo | |
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. (AU) | |
| 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: | 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse |
| Beneficiário: | Fernando de Queiroz Cunha |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |