Fogal Birgit, Hewett Sandra J
Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut, USA.
J Neurochem. 2008 Jul;106(1):1-23. doi: 10.1111/j.1471-4159.2008.05315.x. Epub 2008 Jul 1.
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.
白细胞介素-1(IL-1)是一种由多种细胞类型释放的促炎细胞因子,以自分泌和/或旁分泌方式发挥作用。虽然IL-1被公认为是感染和炎症期间外周免疫反应的重要介质,但越来越多的证据表明IL-1信号传导参与了多种神经系统疾病的发病机制。这种细胞因子导致脑损伤的生化途径在很大程度上仍不明确。在此,我们综述了证明IL-1β在急性和慢性神经系统疾病发病机制中作用的证据。此外,我们强调了一些数据,这些数据使我们提出IL-1β是潜在有益炎症反应与有害谷氨酸兴奋性毒性之间缺失的机制联系。