Glucocorticoids and macrophage migration inhibitory factor (MIF) are neuroendocrine modulators of inflammation and neuropathic pain after spinal cord injury
Publication Date
2014
Journal Title
Semin Immunol
Abstract
Traumatic spinal cord injury (SCI) activates the hypothalamic-pituitary-adrenal (HPA) axis, a potent neuroendocrine regulator of stress and inflammation. SCI also elicits a profound and sustained intraspinal and systemic inflammatory response. Together, stress hormones and inflammatory mediators will affect the growth and survival of neural and non-neural cells and ultimately neurologic recovery after SCI. Glucocorticoids (GCs) are endogenous anti-inflammatory steroids that are synthesized in response to stress or injury, in part to regulate inflammation. Exogenous synthetic GCs are often used for similar purposes in various diseases; however, their safety and efficacy in pre-clinical and clinical SCI is controversial. The relatively recent discovery that macrophage migration inhibitory factor (MIF) is produced throughout the body and can override the anti-inflammatory effects of GCs may provide unique insight to the importance of endogenous and exogenous GCs after SCI. Here, we review both GCs and MIF and discuss the potential relevance of their interactions after SCI, especially their role in regulating maladaptive mechanisms of plasticity and repair that may contribute to the onset and maintenance of neuropathic pain. (C) 2014 Elsevier Ltd. All rights reserved.
Volume Number
26
Issue Number
5
Pages
409-414
Document Type
Article
EPub Date
2014/04/29
Status
Faculty
Facility
School of Medicine
Primary Department
Molecular Medicine
Additional Departments
Physical Medicine and Rehabilitation
PMID
DOI
10.1016/j.smim.2014.03.004