期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 33, 期 -, 页码 1-6出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2013.02.004
关键词
Stress; Priming; Pro-inflammatory; Glucocorticoid; Microglia; Danger; Alarmin
资金
- NIDA NIH HHS [F32 DA015591] Funding Source: Medline
- NIDCR NIH HHS [R01 DE021966] Funding Source: Medline
A considerable number of studies demonstrate that acute and chronic stressors prime CNS innate immune responses to subsequent pro-inflammatory challenges and that glucocorticoids mediate, in part, stress-induced sensitization of pro-inflammatory immune responses. Here, we explore the notion that GCs produce a persisting sensitization of CNS innate immune effectors (e.g. microglia) so that they will generate a potentiated pro-inflammatory response after the GC rise has dissipated, thereby enhancing the sickness response to infection or injury and maximizing the animal's ability to neutralize danger. The stress-induced GC response is conceptualized here as an neuroendocrine warning signal or alarmin to the innate immune system, which prepares or sensitizes the innate immune response to potential danger. Thus, a new understanding of the stress response and its function (priming CNS innate immune responses to infection or injury during a fight/flight emergency) would be suggested. (c) 2013 Elsevier Inc. All rights reserved.
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