Inflammation in epilepsy: Clinical observations
Abstract
Summary: Over the past decade, an increasing number of observations indicate that activation of inflammatory processes occurs in variety of focal epilepsies. Understanding the feature and consequences of neuroinflammation, including the contribution to development and perpetuation of seizures, as well as to mood or cognitive dysfunction, is a major requisite for delineating its role in epilepsy. The present article discusses the most recent observations supporting the involvement of the inflammatory response in human focal epilepsy. It also evaluates emerging evidence concerning the possibility to identify epilepsy‐associated inflammatory biomarkers in cerebrospinal fluid and serum, as well as the potential application of neuroimaging approaches to study the inflammatory reactions in chronic epilepsy patients in vivo, aiming to improve the recognition of appropriate patient populations who might benefit from antiinflammatory or immunomodulatory therapies.
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Astrocytes are a major source and/or targets of pro-epileptogenic inflammatory signaling such as IL-1, HMGB1, and TLR pathways.
“In particular, both in vitro and in vivo data, point to the role of astrocytes as a major source and/or targets of pro-epileptogenic inflammatory signaling, such as the interleukin(IL)-1, High Mobility Group Box 1 (HMGB1) and Toll-like receptor (TLR) signaling pathways [1], [3], [6]–[9].”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [3]
Inflammation is relevant in the pathophysiology of epilepsy.
“During the last decade, both experimental and clinical studies have demonstrated the relevance of inflammation in the pathophysiology of epilepsy (for reviews see [1]–[3].”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [3]
Both the innate and the adaptive immune responses are activated in epilepsy-associated lesions.
“Both the innate and the adaptive immune responses are activated in these lesions ([5]; reviewed in [3]).”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [3]
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Cites
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221 · see citing works
Angiogenesis is associated with blood-brain barrier permeability in temporal lobe epilepsy
Rigau, V., Morin, M., Rousset, M.-C., de Bock, F., Lebrun, A., Coubes, P., Picot, M.-C., Baldy-Moulinier, M., Bockaert, J., Crespel, A., et al. (2007) · Brain · doi:10.1093/brain/awm118 · Cited by 429 · see citing works
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Research works printed but not linked: 1
- Butler T, Ichise M, Teich AF, Gerard E, Osborne J, French J, Devinsky O, Kuzniecky R, Gilliam F, Pervez F, Provenzano F, Goldsmith S, Vallabhajosula S, Stern E, Silbersweig D. (2011) Imaging inflam- mation in a patient with epilepsy due to focal cortical dysplasia. J Neuroimaging. Jan 11. doi: 10.1111/j.1552-6569.2010.00572.x. [Epub ahead of print] · DOI
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Role of microglia in CNS inflammation
Graeber, M. B., Li, W., & Rodriguez, M. L. (2011) · FEBS Letters · doi:10.1016/j.febslet.2011.08.033 · Cited by 392 · see citing works
“‘‘inflammation spectrum’’ of brain disease include epilepsy [59], neurogenesis [60], obesity in mood disorders [61], and alcoholism”
BackgroundMicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response
Iyer, A., Zurolo, E., Prabowo, A., Fluiter, K., Spliet, W. G. M., van Rijen, P. C., Gorter, J. A., & Aronica, E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0044789 · Cited by 330 · see citing works
Self-citation
- Authors
- Aronica, E., & Crino, P. B.
- Venue
- Epilepsia
- Publisher
- Wiley
- Published
- 2011-05
- Volume
- 52
- Issue
- s3
- Pages
- 26-32
- ISSN
- 0013-9580
- 1528-1167
- Cited by
- 272
- References
- 2
- Language
- en
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