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Interleukin‐1β: a bridge between inflammation and excitotoxicity?
Author(s) -
Fogal Birgit,
Hewett Sandra J.
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05315.x
Subject(s) - excitotoxicity , inflammation , proinflammatory cytokine , pathogenesis , autocrine signalling , cytokine , mediator , immunology , neuroscience , immune system , paracrine signalling , interleukin , medicine , glutamate receptor , biology , microbiology and biotechnology , receptor
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.