title: Interleukin-1α and brain inflammation.
abstract: Acute brain injuries such as caused by stroke are amongst the leading causes of death and are the leading cause of disability. Despite this there are very limited therapeutic options, and new therapeutic strategies and targets are required. Inflammation is known to exacerbate brain injury and is now considered as a potential therapeutic target. The damaging inflammation that occurs after acute brain injury is driven by pro-inflammatory members of the interleukin (IL)-1 cytokine family, namely, IL-1α and IL-1β. Previous research efforts have focussed on the biology and contribution of IL-1β. However, we now recognise that IL-1α is an early and important mediator of inflammation after injury. This review focuses on what is known about IL-1α, its regulation and its contribution to brain injury. Inhibiting mechanisms regulating the processing and release of IL-1α may offer new therapeutic targets for the treatment of devastating acute brain injuries.
authors.affiliation: Faculty of Life Sciences, University of Manchester, Manchester, UK.
authors.forename: David
authors.initials: D
authors.lastname: Brough
authors.affiliation: Faculty of Life Sciences, University of Manchester, Manchester, UK.|Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Budapest, Hungary.
authors.forename: Adam
authors.initials: A
authors.lastname: Denes
mesh_terms: D016923:Cell Death; D004660:Encephalitis / Q000503:physiopathology*; D006801:Humans; D053582:Interleukin-1alpha / Q000378:metabolism / Q000502:physiology*
chemical_list: D053582:Interleukin-1alpha
keywords: Ca2+ signalling; cell death; human molecular disease