title: [Inflammation, angiogenesis and epilepsy].
abstract: It is well admitted now that gliosis participates in epileptogenesis, particularly in symptomatic focal epilepsies, like temporal lobe epilepsy. Indeed, astrocytic and microglial activation was shown to release numerous inflammatory factors that modify neuronal excitability or contribute to neuronal loss. These redundant processes maintain chronic epilepsy. However, other sources of inflammation exist. Several studies pointed out the epileptogenicity of blood-brain barrier disruption due to the leakage of leukocytes and serum proteins, triggering inflammatory and immune responses which disturb the neuronal environment. Recently, it was proposed that peripheral inflammation plays a key-role in epilepsy, mainly mediated by circulating cytokines which promote leukocyte extravasation.
authors.affiliation: Institut de Génomique Fonctionnelle, CNRS UMR 5203, INSERM U661, UM1, UM2, 141 rue de la Cardonille, 34094 Montpellier Cedex 9, France. mireille.lerner-natoli@igf.cnrs.fr
authors.forename: Mireille
authors.initials: M
authors.lastname: Lerner-Natoli
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000502:physiology; D001812:Blood-Brain Barrier / Q000503:physiopathology; D016207:Cytokines; D004827:Epilepsy / Q000473:pathology / Q000503:physiopathology; D004833:Epilepsy, Temporal Lobe; D006801:Humans; D007249:Inflammation; D009389:Neovascularization, Pathologic; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000473:pathology
chemical_list: D016207:Cytokines