The Stressed CNS: When Glucocorticoids Aggravate Inflammation

被引:276
作者
Sorrells, Shawn F. [1 ]
Caso, Javier R. [2 ,3 ]
Munhoz, Carolina D. [4 ]
Sapolsky, Robert M. [1 ,2 ,3 ]
机构
[1] Stanford Univ, Dept Biol Sci, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[3] Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA
[4] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508900 Sao Paulo, Brazil
关键词
FACTOR-KAPPA-B; PROTEIN-KINASE PHOSPHATASE-1; OXIDE SYNTHASE EXPRESSION; RESTRAINT STRESS; ACTIVATOR PROTEIN-1; CYTOKINE RESPONSES; CEREBRAL-ISCHEMIA; IMMUNE-RESPONSES; BRAIN CORTEX; RECEPTOR;
D O I
10.1016/j.neuron.2009.09.032
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Glucocorticoids (GCs) are hormones released during the stress response that are well known for their immunosuppressive and anti-inflammatory properties; however, recent advances have uncovered situations wherein they have effects in the opposite direction. The CNS is a particularly interesting example, both because of its unique immune environment, and because GCs affect immune responses differently in different brain regions. In this minireview we discuss the contexts wherein GCs increase CNS inflammation and point out directions for future investigation.
引用
收藏
页码:33 / 39
页数:7
相关论文
共 50 条
[1]  
BARBER AE, 1993, J IMMUNOL, V150, P1999
[2]   Identification of endogenous glucocorticoid repressed genes differentially regulated by a glucocorticoid receptor mutant able to separate between nuclear factor-κB and activator protein-1 repression [J].
Bladh, LG ;
Lidén, J ;
Dahlman-Wright, K ;
Reimers, M ;
Nilsson, S ;
Okret, S .
MOLECULAR PHARMACOLOGY, 2005, 67 (03) :815-826
[3]   Stressor-specific alterations in corticosterone and immune responses in mice [J].
Bowers, Stephanie L. ;
Bilbo, Staci D. ;
Dhabhar, Firdaus S. ;
Nelson, Randy J. .
BRAIN BEHAVIOR AND IMMUNITY, 2008, 22 (01) :105-113
[4]   NF-κB as a therapeutic target in neurodegenerative diseases [J].
Camandola, Simonetta ;
Mattson, Mark P. .
EXPERT OPINION ON THERAPEUTIC TARGETS, 2007, 11 (02) :123-132
[5]  
Cannon WB, 1935, AM J MED SCI, V189, P1
[6]   The role of tumor necrosis factor-alpha in stress-induced worsening of cerebral ischemia in rats [J].
Caso, J. R. ;
Lizasoain, I. ;
Lorenzo, P. ;
Moro, M. A. ;
Leza, J. C. .
NEUROSCIENCE, 2006, 142 (01) :59-69
[7]   Involvement of IL-1β in acute stress-induced worsening of cerebral ischaemia in rats [J].
Caso, Javier R. ;
Moro, Maria A. ;
Lorenzo, Pedro ;
Lizasoain, Ignacio ;
Leza, Juan C. .
EUROPEAN NEUROPSYCHOPHARMACOLOGY, 2007, 17 (09) :600-607
[8]   Crosstalk between glucocorticoids and mitogen-activated protein kinase signalling pathways [J].
Clark, AR ;
Lasa, M .
CURRENT OPINION IN PHARMACOLOGY, 2003, 3 (04) :404-411
[9]   Fast glucocorticoid actions on brain: Back to the future [J].
Dallman, MF .
FRONTIERS IN NEUROENDOCRINOLOGY, 2005, 26 (3-4) :103-108
[10]   The interplay between the glucocorticoid receptor and nuclear factor-κB or activator protein-1:: Molecular mechanisms for gene repression [J].
De Bosscher, K ;
Vanden Berghe, W ;
Haegeman, G .
ENDOCRINE REVIEWS, 2003, 24 (04) :488-522