Leukocyte trafficking mechanisms in epilepsy

被引:50
作者
Fabene, Paolo F. [1 ]
Laudanna, Carlo [2 ]
Constantin, Gabriela [2 ]
机构
[1] Univ Verona, Dept Neurol Neuropsychol Morphol & Movement Sci, Sect Anat, I-37134 Verona, Italy
[2] Univ Verona, Dept Pathol & Diagnost, Sect Gen Pathol, I-37134 Verona, Italy
基金
欧洲研究理事会;
关键词
Leukocyte trafficking; Epilepsy; Seizures; Inflammation; Adhesion molecules; Chemokines; BLOOD-BRAIN-BARRIER; EXPRESSION; ENDOTHELIUM; RECRUITMENT; ALPHA(4)-INTEGRIN; EPILEPTOGENESIS; INFLAMMATION; BREAKDOWN; SEIZURES; PATHWAY;
D O I
10.1016/j.molimm.2012.12.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epilepsy is a chronic disorder that affects 1% of the world population and is characterized by chronically reoccurring seizures. Seizures are initiated by abnormal excessive or synchronous neuronal activity in the brain. Epilepsy requires life long anti-convulsant therapy and current therapies for epilepsy selectively target neuronal activity. In the last decade, cytokines and vascular alterations have been discussed in relation to the pathogenesis of epilepsy, suggesting a potential role for inflammation mechanisms in seizure induction. More recently, it has been shown that leukocyte trafficking plays a key role in seizure generation, and that anti-leukocyte adhesion therapy has therapeutic and preventative effects in an experimental model of human epilepsy. These results were supported by evidence in humans showing that leukocytes accumulate in the brain parenchyma of patients with different types of epilepsy. Finally, recent clinical observations suggest that therapies able to interfere with leukocyte trafficking may have a therapeutic effect in epilepsy. The emerging role for leukocytes and leukocyte adhesion mechanisms in seizure generation provides insight into the mechanisms of brain damage and may contribute to the development of novel therapeutic strategies in epilepsy. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:100 / 104
页数:5
相关论文
共 40 条
[1]   ADHESION MOLECULE EXPRESSION ON MURINE CEREBRAL ENDOTHELIUM FOLLOWING THE INJECTION OF A PROINFLAMMAGEN OR DURING ACUTE NEURONAL DEGENERATION [J].
BELL, MD ;
PERRY, VH .
JOURNAL OF NEUROCYTOLOGY, 1995, 24 (09) :695-710
[2]   Interneurones are not so dormant in temporal lobe epilepsy: a critical reappraisal of the dormant basket cell hypothesis [J].
Bernard, C ;
Esclapez, M ;
Hirsch, JC ;
Bernard, C .
EPILEPSY RESEARCH, 1998, 32 (1-2) :93-103
[3]  
Blamire AM, 2000, J NEUROSCI, V20, P8153
[4]   Inflammatory processes in cortical tubers and subependymal giant cell tumors of tuberous sclerosis complex [J].
Boer, K. ;
Jansen, F. ;
Nellist, M. ;
Redeker, S. ;
van den Ouweland, A. M. W. ;
Spliet, W. G. M. ;
van Nieuwenhuizen, O. ;
Troost, D. ;
Crino, P. B. ;
Aronica, E. .
EPILEPSY RESEARCH, 2008, 78 (01) :7-21
[5]   Loss of the tight junction proteins occludin and zonula occludens-1 from cerebral vascular endothelium during neutrophil-induced blood-brain barrier breakdown in vivo [J].
Bolton, SJ ;
Anthony, DC ;
Perry, VH .
NEUROSCIENCE, 1998, 86 (04) :1245-1257
[6]   The emerging role for chemokines in epilepsy [J].
Fabene, Paolo F. ;
Bramanti, Placido ;
Constantin, Gabriela .
JOURNAL OF NEUROIMMUNOLOGY, 2010, 224 (1-2) :22-27
[7]   A role for leukocyte-endothelial adhesion mechanisms in epilepsy [J].
Fabene, Paolo F. ;
Mora, Graciela Navarro ;
Martinello, Marianna ;
Rossi, Barbara ;
Merigo, Flavia ;
Ottoboni, Linda ;
Bach, Simona ;
Angiari, Stefano ;
Benati, Donatella ;
Chakir, Asmaa ;
Zanetti, Lara ;
Schio, Federica ;
Osculati, Antonio ;
Marzola, Pasquina ;
Nicolato, Elena ;
Homeister, Jonathon W. ;
Xia, Lijun ;
Lowe, John B. ;
McEver, Rodger P. ;
Osculati, Francesco ;
Sbarbati, Andrea ;
Butcher, Eugene C. ;
Constantin, Gabriela .
NATURE MEDICINE, 2008, 14 (12) :1377-1383
[8]   Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine-induced status epilepticus [J].
Foresti, Maira L. ;
Arisi, Gabriel M. ;
Katki, Khurshed ;
Montanez, Andres ;
Sanchez, Russell M. ;
Shapiro, Lee A. .
JOURNAL OF NEUROINFLAMMATION, 2009, 6
[9]   Signaling via β2 integrins triggers neutrophil-dependent alteration in endothelial barrier function [J].
Gautam, N ;
Herwald, H ;
Hedqvist, P ;
Lindbom, L .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 191 (11) :1829-1839
[10]   Lymphocyte migration into the central nervous system: Implication of ICAM-1 signalling at them blood-brain barrier [J].
Greenwood, J ;
Etienne-Manneville, S ;
Adamson, P ;
Couraud, PO .
VASCULAR PHARMACOLOGY, 2002, 38 (06) :315-322