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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Frontline Science: Blood-circulating leukocytes fail to infiltrate the spinal cord parenchyma after spared nerve injury

Texto completo
Autor(es):
Guimaraesi, Rafaela M. [1, 2] ; Davoli-Ferreira, Marcela [1, 2] ; Fonseca, Miriam M. [1, 3] ; Damasceno, Luis Eduardo A. [1, 2] ; Santa-Cecilia, V, Flavia ; Kusuda, Ricardo [4] ; Menezes, Gustavo B. [5] ; Cunha, Fernando Q. [4] ; Alves-Filho, Jose C. [4] ; Cunha, Thiago M. [4]
Número total de Autores: 10
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, CRID, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Ribeirao Preto Med Sch, Grad Program Basic & Appl Immunol, Ribeirao Preto, SP - Brazil
[3] Wake Forest Univ, Bowman Gray Sch Med, Dept Anesthesiol, Pain Mech Lab, Winston Salem, NC - USA
[4] Santa-Cecilia, Flavia, V, Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, CRID, Ribeirao Preto, SP - Brazil
[5] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Morfol, Ctr Gastrointestinal Biol, Belo Horizonte, MG - Brazil
Número total de Afiliações: 5
Tipo de documento: Artigo Científico
Fonte: Journal of Leukocyte Biology; v. 106, n. 3, SI, p. 541-551, SEP 2019.
Citações Web of Science: 1
Resumo

The development of neuropathic pain after peripheral nerve injury involves neuroimmune-glial interactions in the spinal cord. However, whether the development of neuropathic pain depends on the infiltration of peripheral immune cells, such as monocytes, into the spinal cord parenchyma after peripheral nerve damage remains unclear. Here, we used a combination of different techniques such as transgenic reporter mouse (Cx3cr1(GFP/+) and Ccr2(RFP/+) mice), bone marrow chimeric mice, and parabiosis to investigate this issue in spared nerve injury (SNI) model. Herein, we provided robust evidence that, although microglial cells are activated/proliferate at the dorsal horn of the spinal cord after SNI, peripheral hematopoietic cells (including monocytes) are not able to infiltrate into the spinal cord parenchyma. Furthermore, there was no evidence of CCR2 expression in intrinsic cells of the spinal cord. However, microglial cells activation/proliferation in the spinal cord and mechanical allodynia after SNI were reduced in Ccr2-deficient mice. These results suggest that blood-circulating leukocytes cells are not able to infiltrate the spinal cord parenchyma after distal peripheral nerve injury. Nevertheless, they indicate that CCR2-expressing cells might be indirectly regulating microglia activation/proliferation in the spinal cord after SNI. In conclusion, our study supports that CCR2 inhibition could be explored as an interventional approach to reduce microglia activation and consequently 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
Linha de fomento: 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
Linha de fomento: Auxílio à Pesquisa - Temático