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Mol Neurobiol. 2016 Nov;53(9):6540-6547. doi: 10.1007/s12035-015-9552-0. Epub 2015 Nov 28.

IL-1β Is Involved with the Generation of Pain in Experimental Autoimmune Encephalomyelitis.

Author information

1
Department of Basic and Health Sciences, Universidade Federal de Juiz de Fora-campus Governador Valadares, de Juiz de Fora, Brazil. dhenrodrigues@gmail.com.
2
Translational Psychoneuroimmunology Group, Laboratory of Immunopharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. dhenrodrigues@gmail.com.
3
Department of Biochemistry, Universidade Federal de Minas Gerais, Belo Horizonte, MG, 31270-901, Brazil. dhenrodrigues@gmail.com.
4
Department of Biochemistry, Universidade Federal de Minas Gerais, Belo Horizonte, MG, 31270-901, Brazil.
5
Translational Psychoneuroimmunology Group, Laboratory of Immunopharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Abstract

Pain is one of the main symptoms of multiple sclerosis, a demyelinating disease of the central nervous system that affects millions of people worldwide. The experimental autoimmune encephalomyelitis (EAE) is considered an experimental model of multiple sclerosis, and besides motor weakness, hypernociception is one of the clinical signs of animals with EAE. In this study, we investigated the influence of some cytokines in the generation of the hypernociceptive response in a mouse model of EAE using MOG35-55. We measured some cytokines in the dorsal root ganglia (DRG), an important anatomical structure involved in pain. We found increased levels of the cytokines TNF-α, IL-1β, and Kc in DRGs of animals with EAE. We used the antibody IL-1ra to antagonize the effects of IL-1β, and animals presented a decrease in the hypernociceptive response. Thus, our results suggest that hypernociception in this experimental model of EAE may be a consequence of the increase in some cytokines in DRGs, especially IL-1β.

KEYWORDS:

Cytokines; Dorsal root ganglia; Experimental autoimmune encephalomyelitis; Hypernociception

PMID:
26614512
DOI:
10.1007/s12035-015-9552-0
[Indexed for MEDLINE]

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