Interleukin‐1β: 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‐1β to the pathogenesis of both acute and chronic neurological disorders. Further, we highlight data that leads us to propose IL‐1β as the missing mechanistic link between a potential beneficial inflammatory response and detrimental glutamate excitotoxicity.