Glia as a source of cytokines: Implications for neuronal excitability and survival
Abstract
Summary: In the last decade, preclinical studies have provided a better characterization of the homeostatic and maladaptive mechanisms occurring either during the process of epileptogenesis or after the permanent epileptic state has emerged. Experimental evidence supported by clinical observations highlighted the possibility that brain inflammation is a common factor contributing, or predisposing, to the occurrence of seizures and cell death, in various forms of epilepsy of different etiologies. Expression of proinflammatory cytokines, as a hallmark of brain inflammation, has been demonstrated in glia in various experimental models of seizures and in human epilepsies. Experimental studies in rodents with perturbed cytokine systems indicate that these inflammatory mediators can alter neuronal excitability and affect cell survival by activating transcriptional and posttranslational intracellular pathways. This paper will provide an overview on the current knowledge in this field to discuss mechanistic hypotheses into the study of pathogenesis of epilepsy and recognize new potential therapeutic options.
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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 [1]
The ‘Cytokines in Human Epileptic Tissue’ section (page not supplied) reports that astrocytes express IL-1β and its receptor, supporting their role as sources and targets of IL-1 signaling. The ‘Concluding Remarks’ describe the IL-1β–IL-1R1 system as a potentially harmful pathway in epileptogenesis. The supplied passages and searches do not establish the claimed astrocyte roles in HMGB1 or TLR signaling. (LLM, conf=0.88)
Experimental — accuracy not yet measuredInflammation 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 [1]
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Cites
Fujiwara, N., & Kobayashi, K. (2005) · Current Drug Target -Inflammation & Allergy · doi:10.2174/1568010054022024 · Cited by 1,420 · cited 1× · see citing works
“…were present in areas of neuronal loss in human epileptic tissue as well as in experimental models, suggesting that these cells may contribute to neuronal injury by releasing cytotoxic mediators including cytokines (Cassatella, 1999; Fujiwara & Kobayashi, 2005) and glutamate (Piani et al., 1991).”
BackgroundControl of Synaptic Strength by Glial TNFα
Beattie, E. C., Stellwagen, D., Morishita, W., Bresnahan, J. C., Ha, B. K., Von Zastrow, M., Beattie, M. S., & Malenka, R. C. (2002) · Science · doi:10.1126/science.1067859 · Cited by 1,344 · see citing works
Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α
Stellwagen, D., Beattie, E. C., Seo, J. Y., & Malenka, R. C. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.4486-04.2005 · Cited by 985 · cited 1× · see citing works
“Proictogenic effects induced by brain inflammation have been reported also in rodents exposed to lipopolysaccaride (LPS), a bacterial toxin, (Sayyah et al., 2003) or to specific pathogens mimicking systemic infection (Yuhas et al., 1999; Stringer et al., 2003; Meli et al., 2004).”
BackgroundNovel glucocorticoid effects on acute inflammation in the CNS
Dinkel, K., MacPherson, A., & Sapolsky, R. M. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01604.x · Cited by 179 · see citing works
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Research works printed but not linked: 1
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Microglia activation triggers astrocyte-mediated modulation of excitatory neurotransmission
Pascual, O., Ben Achour, S., Rostaing, P., Triller, A., & Bessis, A. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1111098109 · Cited by 693 · see citing works
The impact of microglial activation on blood-brain barrier in brain diseases
da Fonseca, A. C. C., Matias, D., Garcia, C., Amaral, R., Geraldo, L. H., Freitas, C., & Lima, F. R. S. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00362 · Cited by 572 · see citing works
Antonucci, F., Turola, E., Riganti, L., Caleo, M., Gabrielli, M., Perrotta, C., Novellino, L., Clementi, E., Giussani, P., Viani, P., et al. (2012) · The EMBO Journal · doi:10.1038/emboj.2011.489 · Cited by 328 · see citing works
MicroRNA-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-citationRecent advances in psychoneuroimmunology: Inflammation in psychiatric disorders
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- Authors
- Vezzani, A., Ravizza, T., Balosso, S., & Aronica, E.
- Venue
- Epilepsia
- Publisher
- Wiley
- Published
- 2008-01-22
- Volume
- 49
- Issue
- s2
- Pages
- 24-32
- ISSN
- 0013-9580
- 1528-1167
- Cited by
- 173
- References
- 4
- Language
- en
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