Role of Microglia in Neurotrauma

被引:539
作者
Loane, David J. [2 ,3 ]
Byrnes, Kimberly R. [1 ]
机构
[1] Uniformed Serv Univ Hlth Sci, Dept Anat Physiol & Genet, Bethesda, MD 20814 USA
[2] Univ Maryland, Dept Anesthesiol, Sch Med, Baltimore, MD 21201 USA
[3] Univ Maryland, Sch Med, Ctr Shock Trauma & Anesthesiol Res STAR, Natl Study Ctr Trauma & EMS, Baltimore, MD 21201 USA
关键词
Microglia; spinal cord injury; traumatic brain injury; inflammation; SPINAL-CORD-INJURY; TRAUMATIC BRAIN-INJURY; TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1 RECEPTOR ANTAGONIST; PPAR-GAMMA AGONISTS; INTRACEREBRAL INFLAMMATORY RESPONSE; METABOTROPIC GLUTAMATE RECEPTORS; IMPROVES FUNCTIONAL RECOVERY; MACROPHAGE-GENE-EXPRESSION; AMYLOID PROTEIN DEPOSITION;
D O I
10.1016/j.nurt.2010.07.002
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Microglia are the primary mediators of the immune defense system of the CNS and are integral to the subsequent inflammatory response. The role of microglia in the injured CNS is under scrutiny, as research has begun to fully explore how postinjury inflammation contributes to secondary damage and recovery of function. Whether microglia are good or bad is under debate, with strong support for a dual role or differential activation of microglia. Microglia release a number of factors that modulate secondary injury and recovery after injury, including pro-and anti-inflammatory cytokines, chemokines, nitric oxide, prosta-glandins, growth factors, and superoxide species. Here we review experimental work on the complex and varied responses of microglia in terms of both detrimental and beneficial effects. Addressed in addition are the effects of microglial activation in two examples of CNS injury: spinal cord and traumatic brain injury. Microglial activation is integral to the response of CNS tissue to injury. In that light, future research is needed to focus on clarifying the signals and mechanisms by which microglia can be guided to promote optimal functional recovery.
引用
收藏
页码:366 / 377
页数:12
相关论文
共 202 条
[1]  
Aggarwal B.B., 2001, Cytokine reference. A compendium of cytokines and another mediator of host defense, VVol I, P413
[2]   Spatial and temporal gene expression profiling of the contused rat spinal cord [J].
Aimone, JB ;
Leasure, JL ;
Perreau, VM ;
Thallmair, M .
EXPERIMENTAL NEUROLOGY, 2004, 189 (02) :204-221
[3]   Microarray analysis of activated mixed glial (microglia) and monocyte-derived macrophage gene expression [J].
Albright, AV ;
González-Scarano, F .
JOURNAL OF NEUROIMMUNOLOGY, 2004, 157 (1-2) :27-38
[4]   Interleukin-1 and neuronal injury [J].
Allan, SM ;
Tyrrell, PJ ;
Rothwell, NJ .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (08) :629-640
[5]   Immune function of microglia [J].
Aloisi, F .
GLIA, 2001, 36 (02) :165-179
[6]  
Aloisi F, 1999, J NEUROSCI RES, V56, P571
[7]   Microglia and Microglia-Like Cell Differentiated from DC Inhibit CD4 T Cell Proliferation [J].
Bai, Bo ;
Song, Wengang ;
Ji, Yewei ;
Liu, Xi ;
Tian, Lei ;
Wang, Chao ;
Chen, Dongwei ;
Zhang, Xiaoning ;
Zhang, Minghui .
PLOS ONE, 2009, 4 (11)
[8]   Anti-CD11d antibody treatment reduces free radical formation and cell death in the injured spinal cord of rats [J].
Bao, F ;
Dekaban, GA ;
Weaver, LC .
JOURNAL OF NEUROCHEMISTRY, 2005, 94 (05) :1361-1373
[9]   Peroxynitrite generated in the rat spinal cord induces neuron death and neurological deficits [J].
Bao, F ;
Liu, D .
NEUROSCIENCE, 2002, 115 (03) :839-849
[10]   Inflammation, degeneration and regeneration in the injured spinal cord: insights from DNA microarrays [J].
Bareyre, FM ;
Schwab, ME .
TRENDS IN NEUROSCIENCES, 2003, 26 (10) :555-563