Investigation of the protective role of interleukin 27 (IL-27) on the genesis and maintenance of neuropathic pain

• Grant number: 13/15316-3
• Support Opportunities: Scholarships in Brazil - Doctorate
• Effective date (Start): January 01, 2014
• Effective date (End): May 31, 2017
• Field of knowledge: Biological Sciences - Pharmacology - General Pharmacology
• Principal Investigator: Thiago Mattar Cunha
• Grantee: Miriam das Dores Mendes Fonseca
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated research grant: 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis, AP.TEM

Abstract

Chronic pain is a public health problem which affects negatively the quality of life of patients. Despite major advances in recent years in the treatment of chronic pain, the mechanisms involved in the induction and maintenance of chronic painful process are still poorly understood. Neuropathic pain occurs as a direct result of illness or injury affecting the somatosensory system. There is increasing evidence that the interaction between the immune system and the nervous system plays a key role in the pathophysiology of chronic pain. Thus, neuroinflammation mediated by activation of glial cells (astrocytes and microglia) and the peripheral immune system and deregulation in the production of pro-inflammatory and anti-inflammatory mediators contribute to the generation and maintenance of neuropathic pain. Cells that participate in neuroinflammation, and produce pro-inflammatory components can produce anti-inflammatory mediators that negatively regulate the process, among them stand anti-inflammatory cytokines. A cytokine, recently described in the literature with this property is the interleukin IL-27. In inflammatory conditions in the central nervous system, IL-27 is produced promoting system protection, regulating exacerbated inflammation. However, no study has reported the role of IL-27 in response to neuroimmune neuropathic pain. Therefore, the hypothesis of this project is that during neuroimmune activation, caused by nerve injury, the IL-27 present anti-inflammatory functions, acting as a protective component in the genesis and/or maintenance of neuropathic pain, negatively regulating the inflammatory response mediated by glial cells (microglia and astrocytes).