Astrocyte immune responses in epilepsy

被引:178
作者
Aronica, Eleonora [1 ,2 ]
Ravizza, Teresa [3 ]
Zurolo, Emanuele [1 ]
Vezzani, Annamaria [3 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, Dept Neuro Pathol, NL-1105 AZ Amsterdam, Netherlands
[2] Netherlands Fdn Stichting Epilepsie Instellingen, Epilepsy Inst, Heemstede, Netherlands
[3] Mario Negri Inst Pharmacol Res, Milan, Italy
关键词
human; rodents; epilepsy; astrocytes; inflammation; cytokines; TEMPORAL-LOBE EPILEPSY; TUBEROUS SCLEROSIS COMPLEX; CENTRAL-NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER; NF-KAPPA-B; CULTURED HUMAN ASTROCYTES; ANTIGEN-PRESENTING CELLS; NECROSIS-FACTOR-ALPHA; TOLL-LIKE-RECEPTORS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
D O I
10.1002/glia.22312
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Astrocytes, the major glial cell type of the central nervous system (CNS), are known to play a major role in the regulation of the immune/inflammatory response in several human CNS diseases. In epilepsy-associated pathologies, the presence of astrogliosis has stimulated extensive research focused on the role of reactive astrocytes in the pathophysiological processes that underlie the development of epilepsy. In brain tissue from patients with epilepsy, astrocytes undergo significant changes in their physiological properties, including the activation of inflammatory pathways. Accumulating experimental evidence suggests that proinflammatory molecules can alter glio-neuronal communications contributing to the generation of seizures and seizure-related neuronal damage. In particular, both in vitro and in vivo data point to the role of astrocytes as both major source and target of epileptogenic inflammatory signaling. In this context, understanding the astroglial inflammatory response occurring in epileptic brain tissue may provide new strategies for targeting astrocyte-mediated epileptogenesis. This article reviews current evidence regarding the role of astrocytes in the regulation of the innate immune responses in epilepsy. Both clinical observations in drug-resistant human epilepsies and experimental findings in clinically relevant models will be discussed and elaborated, highlighting specific inflammatory pathways (such as interleukin-1 beta/toll-like receptor 4) that could be potential targets for antiepileptic, disease-modifying therapeutic strategies. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:1258 / 1268
页数:11
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