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

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 proce...

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Published inFrontiers 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
LanguageEnglish
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
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Abstract 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.
AbstractList 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.
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.
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.
Author Guimarães, Rafaela M
Oliveira, Francisco F B
Santa-Cecília, Flávia
Alves-Filho, José C
Davoli-Ferreira, Marcela
Kusuda, Ricardo
Ferreira, David W
Cunha, Fernando Q
Fonseca, Miriam M
Cunha, Thiago M
AuthorAffiliation 1 Department of Pharmacology, Center for Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo (USP) , Ribeirão Preto , Brazil
2 Graduate Program in Basic and Applied Immunology, Ribeirão Preto Medical School, University of São Paulo (USP) , Ribeirão Preto , Brazil
AuthorAffiliation_xml – name: 1 Department of Pharmacology, Center for Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo (USP) , Ribeirão Preto , Brazil
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  givenname: David W
  surname: Ferreira
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Copyright Copyright © 2020 Fonseca, Davoli-Ferreira, Santa-Cecília, Guimarães, Oliveira, Kusuda, Ferreira, Alves-Filho, Cunha and Cunha.
Copyright © 2020 Fonseca, Davoli-Ferreira, Santa-Cecília, Guimarães, Oliveira, Kusuda, Ferreira, Alves-Filho, Cunha and Cunha. 2020 Fonseca, Davoli-Ferreira, Santa-Cecília, Guimarães, Oliveira, Kusuda, Ferreira, Alves-Filho, Cunha and Cunha
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Keywords IL-27
glial cells
macrophages
neuropathic pain
cytokines
IL-10
Language English
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This article was submitted to Multiple Sclerosis and Neuroimmunology, a section of the journal Frontiers in Immunology
Edited by: Felipe Almeida Pinho Ribeiro, Harvard Medical School, United States
Present address: Miriam M. Fonseca, Pain Mechanisms Laboratory, Department of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, NC, United States
Reviewed by: Felipe J. Nobre Lelis, Brigham and Women's Hospital and Harvard Medical School, United States; Rafael Gonzalez-Cano, Boston Children's Hospital and Harvard Medical School, United States; Larissa Staurengo-Ferrari, University of California, San Francisco, United States
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Snippet Neuroimmune-glia interactions have been implicated in the development of neuropathic pain. Interleukin-27 (IL-27) is a cytokine that presents regulatory...
Neuroimmune–glia interactions have been implicated in the development of neuropathic pain. Interleukin-27 (IL-27) is a cytokine that presents regulatory...
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StartPage 3059
SubjectTerms cytokines
glial cells
IL-10
IL-27
Immunology
macrophages
neuropathic pain
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Title IL-27 Counteracts Neuropathic Pain Development Through Induction of IL-10
URI https://www.ncbi.nlm.nih.gov/pubmed/32047492
https://search.proquest.com/docview/2354163008
https://pubmed.ncbi.nlm.nih.gov/PMC6997342
https://doaj.org/article/9d29671462ae4393ba0ae6f5d8f3cd14
Volume 10
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