The role of inflammation is increasingly recognized in triggering or sustaining epileptic activity. In the last decades, increasing research has provided definite evidence to support the link between immunity, inflammatory process, and epilepsy. Neuro- and systemic inflammation play a pivotal role in driving epileptogenesis through different pathogenetic mechanisms: the activation of innate immunity in glia, neurons, and microvasculature, the brain mediated by blood-brain barrier (BBB) impairment, and the imbalance of pro- and anti-inflammatory molecules produced by both arms of immunity. More recently, research has focused on the adverse effects of maternal or early-life immune activation and cytokine imbalance on fetal neurodevelopment and postnatal epilepsy. A complex crosstalk between the immune and nervous system, and a crucial interplay of genetic, epigenetic, and environmental factors may influence structures and functions of the developing brain. A better understanding of the inflammatory process in promoting epilepsy implies that targeting specific pathways may be effective in seizure control. Multiple targets have been identified so far, and several antiseizure interventions are obtained by inhibiting inflammatory signaling or protecting/restoring BBB. All this evidence has changed the field of epilepsy research and neuropharmacology. Further developments and new treatments will rapidly emerge to improve seizure management in inflammation-related epilepsies. This article is part of the Special Issue "Severe Infantile Epilepsies".
Keywords: Encephalitis; Epilepsy; Epileptogenesis; Immunity; Neurodevelopment; Neuroinflammation.
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