IL-1β Is Involved with the Generation of Pain in Experimental Autoimmune Encephalomyelitis
David Henrique Rodrigues1,2,3, Bruno Pereira Leles4, Vivian Vasconcelos Costa4
1Department of Basic and Health Sciences, Universidade Federal de Juiz de Fora-campus Governador Valadares, de Juiz de Fora, Brazil. dhenrodrigues@gmail.com.
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.
