title: In-situ expression of Interleukin-18 and associated mediators in the human brain of sALS patients: Hypothesis for a role for immune-inflammatory mechanisms.
abstract: Recent studies reported over-expression of a cytokine (Interleukin (IL)-18) in the serum of sporadic amyotrophic lateral sclerosis (sALS) patients. Here, we report on the first-time detection of in-situ expression of activated IL-18 in the human brain in sALS patients. We also detected cerebral in-situ expression of key-molecules known to be closely related to the molecular network associated with the activation/secretion of IL-18 cytokine, namely, the receptor-interacting serine/threonine-protein kinase 3 (RIPK3 or RIP3), NOD-like receptor pyrin domain containing 3 (NLRP3)-inflammasome, and activated caspase-1. These findings suggest and allow to hypothesize that there might be a role for this cytokine network in molecular mechanisms associated with or implicated in the physiopathology of this neurodegenerative disorder.
authors.affiliation: Neuropathology Unit, and Reference Center for Neuromuscular Pathology, Brugmann University Hospital (CHU-Brugmann), Université Libre de Bruxelles (U.L.B.), Brussels, Belgium. Electronic address: Hazim.Kadhim@chu-brugmann.be.
authors.forename: Hazim
authors.initials: H
authors.lastname: Kadhim
authors.affiliation: Department of Neurology, CHU Brugmann, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium.
authors.forename: Paul
authors.initials: P
authors.lastname: Deltenre
authors.affiliation: Department of Neurology (Antwerp University Hospital) and Born-Bunge Institute (Antwerp University), Antwerp, Belgium.
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Martin
authors.affiliation: Child Neurology, Montreal Children Hospital, McGill University, Montreal, Canada.
authors.forename: Guillaume
authors.initials: G
authors.lastname: Sébire
mesh_terms: D000690:Amyotrophic Lateral Sclerosis / Q000276:immunology*; D001921:Brain / Q000276:immunology*; D004660:Encephalitis / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology*; D020382:Interleukin-18 / Q000276:immunology*; D018448:Models, Immunological; D008959:Models, Neurological
chemical_list: D018836:Inflammation Mediators; D020382:Interleukin-18