title: Interleukin-1beta: a bridge between inflammation and excitotoxicity?
abstract: Interleukin-1 (IL-1) is a proinflammatory cytokine released by many cell types that acts in both an autocrine and/or paracrine fashion. While IL-1 is best described as an important mediator of the peripheral immune response during infection and inflammation, increasing evidence implicates IL-1 signaling in the pathogenesis of several neurological disorders. The biochemical pathway(s) by which this cytokine contributes to brain injury remain(s) largely unidentified. Herein, we review the evidence that demonstrates the contribution of IL-1beta to the pathogenesis of both acute and chronic neurological disorders. Further, we highlight data that leads us to propose IL-1beta as the missing mechanistic link between a potential beneficial inflammatory response and detrimental glutamate excitotoxicity.
authors.affiliation: Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut, USA.
authors.forename: Birgit
authors.initials: B
authors.lastname: Fogal
authors.forename: Sandra J
authors.initials: SJ
authors.lastname: Hewett
mesh_terms: D002352:Carrier Proteins / Q000276:immunology / Q000378:metabolism; D002493:Central Nervous System Diseases / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism*; D008297:Male; D009498:Neurotoxins / Q000378:metabolism* / Q000633:toxicity; D018384:Oxidative Stress / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology
chemical_list: D002352:Carrier Proteins; D053583:Interleukin-1beta; D009498:Neurotoxins