IL-1[beta] Is Involved with the Generation of Pain in Experimental Autoimmune Encephalomyelitis

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, hypernoc...

Full description

Saved in:
Bibliographic Details
Published in:Molecular neurobiology 2016-11, Vol.53 (9), p.6540
Main Authors: Rodrigues, David Henrique, Leles, Bruno Pereira, Costa, Vivian Vasconcelos, Miranda, Aline Silva, Cisalpino, Daniel, Gomes, Dawidson Assis, de Souza, Danielle Glória, Teixeira, Antônio Lúcio
Format: Article
Language:English
Subjects:
Autoimmune diseases
Cytokines
Multiple sclerosis
Nervous system
Neurobiology
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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-[alpha], IL-1[beta], and Kc in DRGs of animals with EAE. We used the antibody IL-1ra to antagonize the effects of IL-1[beta], 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-1[beta].
ISSN:0893-7648
1559-1182
DOI:10.1007/s12035-015-9552-0