The role of interleukin-1 in seizures and epilepsy: A critical review

被引:87
作者
Rijkers, K. [1 ,2 ]
Majoie, H. J. [3 ,4 ]
Hoogland, G. [1 ,2 ]
Kenis, G. [2 ]
De Baets, M. [2 ]
Vles, J. S. [5 ]
机构
[1] Univ Med Ctr, Dept Neurosurg, NL-6202 AZ Maastricht, Netherlands
[2] Maastricht Univ, Sch Mental Hlth & Neurosci, Dept Psychiat & Neuropsychol, Maastricht, Netherlands
[3] Epilepsy Ctr Kempenhaeghe, Dept Neurol, Heeze, Netherlands
[4] Univ Med Ctr, Dept Neurol, Maastricht, Netherlands
[5] Univ Med Ctr, Dept Child Neurol, Maastricht, Netherlands
关键词
Epilepsy; Seizures; Interleukin-1; Review; TEMPORAL-LOBE EPILEPSY; TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; MESSENGER-RNA LEVELS; FACTOR-KAPPA-B; IL-1 RECEPTOR ANTAGONIST; ACTIVATED PROTEIN-KINASE; INCREASED PLASMA-LEVELS; KAINIC ACID; FACTOR-ALPHA;
D O I
10.1016/j.expneurol.2008.12.014
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Interleukin-1 (IL-1) has a multitude of functions in the central nervous system. Some of them involve mechanisms that are related to epileptogenesis. The role of IL-1 in seizures and epilepsy has been investigated in both patients and animal models. This review aims to synthesize, based on the currently available literature, the consensus role of IL-1 in epilepsy. Three lines of evidence suggest a role for IL-1: brain tissue from epilepsy patients and brain tissue from animal models shows increased IL-1 expression after seizures, and IL-1 has proconvulsive properties when applied excigeneously. However, opposing results have been published as well. More research is needed to fully establish the role of IL-1 in seizure generation and epilepsy, and to explore possible new treatment strategies that are based on interference with intracellular signaling cascades that are initiated when IL-1 binds to its receptor. (c) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:258 / 271
页数:14
相关论文
共 152 条
[1]
Inflammation in central nervous system injury [J].
Allan, SM ;
Rothwell, NJ .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2003, 358 (1438) :1669-1677
[2]
Cytokines and acute neurodegeneration [J].
Allan, SM ;
Rothwell, NJ .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (10) :734-744
[3]
Interleukin-1 and neuronal injury [J].
Allan, SM ;
Tyrrell, PJ ;
Rothwell, NJ .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (08) :629-640
[4]
Impaired interleukin-1 signaling is associated with deficits in hippocampal memory processes and neural plasticity [J].
Avital, A ;
Goshen, I ;
Kamsler, A ;
Segal, M ;
Iverfeldt, K ;
Richter-Levin, G ;
Yirmiya, R .
HIPPOCAMPUS, 2003, 13 (07) :826-834
[5]
Gene expression analysis reveals altered brain transcription of glutamate receptors and inflammatory genes in a patient with chronic focal (Rasmussen's) encephalitis [J].
Baranzini, SE ;
Laxer, K ;
Bollen, A ;
Oksenberg, JR .
JOURNAL OF NEUROIMMUNOLOGY, 2002, 128 (1-2) :9-15
[6]
Transforming growth factor β1 prevents IL-1β-induced microglial activation, whereas TNFα- and IL-6-stimulated activation are not antagonized [J].
Basu, A ;
Krady, JK ;
Enterline, JR ;
Levison, SW .
GLIA, 2002, 40 (01) :109-120
[7]
DEMONSTRATION OF INTERLEUKIN-1-BETA IN LEWIS RAT-BRAIN DURING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY IMMUNOCYTOCHEMISTRY AT THE LIGHT AND ULTRASTRUCTURAL LEVEL [J].
BAUER, J ;
BERKENBOSCH, F ;
VANDAM, AM ;
DIJKSTRA, CD .
JOURNAL OF NEUROIMMUNOLOGY, 1993, 48 (01) :13-22
[8]
Bertolani MF, 1996, CHILD NERV SYST, V12, P534
[9]
Cytokine induction of inducible nitric oxide synthase in an oligodendrocyte cell line: Role of p38 mitogen-activated protein kinase activation [J].
Bhat, NR ;
Zhang, PS ;
Bhat, AN .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (02) :472-478
[10]
Epilepsy induced by extended amygdala-kindling in rats:: lack of clear association between development of spontaneous seizures and neuronal damage [J].
Brandt, C ;
Ebert, U ;
Löscher, W .
EPILEPSY RESEARCH, 2004, 62 (2-3) :135-156