The Potential Role of Pro-Inflammatory and Anti-Inflammatory Cytokines in Epilepsy Pathogenesis

(E-pub Ahead of Print)

Author(s): Ali N. Kamali, Zeineb Zian, José M. Bautista, Haleh Hamedifar, Nikoo Hossein-Khannazer, Ramin Hosseinzadeh, Reza Yazdani, Gholamreza Azizi*

Journal Name: Endocrine, Metabolic & Immune Disorders - Drug Targets
Formerly Current Drug Targets - Immune, Endocrine & Metabolic Disorders

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Within the pathophysiology of epilepsy, as a chronic brain disorder, neuroinflammation has been extensively implied. Recurrent seizures of epilepsy have been associated with elevated levels of immune mediators that seem to play a pivotal role in triggering them. Neurons, glia, and endothelial cells of the blood-brain barrier (BBB) take part in such inflammatory processes by expressing receptors of associated mediators through autocrine and paracrine stimulation of intracellular signaling pathways. In this milieu, elevated cytokine levels in serum and brain tissue have been reported in patients with an epileptic profile. Noteworthy, interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) are the proinflammatory cytokines mostly associated, in literature, with the pathogenesis of epilepsies. In this review, we examine the function of these cytokines in connection with transforming growth factor-beta (TGF-β), IL-8, IL-12, IL-18, and macrophage inflammatory protein (MIP) as potential proinflammatory mediators in the neuropathology of epilepsy.

Keywords: Epilepsy, seizure, neuroinflammation, proinflammatory mediators, cytokine.

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Article Details

Published on: 16 November, 2020
(E-pub Ahead of Print)
DOI: 10.2174/1871530320999201116200940
Price: $95

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