stress-induced neuroinflammatory priming: a liability factor in the etiology of psychiatric disorders

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ID: 234010
2016
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Abstract
Stress and glucocorticoids (GCs) have universally been considered to be anti-inflammatory, however in recent years, stress and GCs have been found to exert permissive effects (immunological priming) on neuroinflammatory processes. This phenomenon of priming is characterized by prior stress or GC exposure potentiating the neuroinflammatory response to a subsequent immune challenge. A considerable body of evidence is discussed here that supports this permissive effect of stress and GCs. In light of this evidence, a mechanism of neuroinflammatory priming is proposed involving a signal cascade in the brain involving danger-associated molecular patterns (HMGB-1) and inflammasomes (NLRP3), which results in an exaggerated or amplified neuroinflammatory response and subsequently, the amplification of the physiological and behavioral sequelae of this response (i.e. sickness). Finally, we explore the notion that stressor-induced sensitization of the neuroimmune microenvironment may predispose individuals to psychiatric disorders, in which exaggerated innate immune/inflammatory responses in the brain are now thought to play a key role.
Reference Key
frank2016neurobiologystress-induced Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Matthew G. Frank;Michael D. Weber;Linda R. Watkins;Steven F. Maier
Journal Environmental science & technology
Year 2016
DOI
10.1016/j.ynstr.2015.12.004
URL
http://www.sciencedirect.com/science/article/pii/S2352289515300308
Keywords
stress priming microglia neuroinflammation glucocorticoids neuropsychiatryneurology biological psychiatry diseases of the nervous systemneurophysiology and neuropsychology hmgb-1neurosciences

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