Interleukin‐1β: a bridge between inflammation and excitotoxicity?
- 25 February 2008
- journal article
- review article
- Published by Wiley in Journal of Neurochemistry
- Vol. 106 (1), 1-23
- https://doi.org/10.1111/j.1471-4159.2008.05315.x
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.Keywords
This publication has 103 references indexed in Scilit:
- Causes of oxidative stress in Alzheimer diseaseCellular and Molecular Life Sciences, 2007
- Endogenous Interleukin-1 Receptor Antagonist is NeuroprotectiveBiochemical and Biophysical Research Communications, 1997
- Interleukin-1β, interleukin-6, epidermal growth factor and transforming growth factor-α are elevated in the brain from parkinsonian patientsNeuroscience Letters, 1994
- Non-classical glutamate receptors, blocked by both NMDA and non-NMDA antagonists, stimulate nitric oxide production in neuronsNeuropharmacology, 1993
- Heterogeneity of high affinity uptake of L-glutamate and L-aspartate in the mammalian central nervous systemLife Sciences, 1992
- Pretreatment with NMDA antagonists limits release of excitatory amino acids following traumatic brain injuryNeuroscience Letters, 1992
- Blocking IL-1: interleukin 1 receptor antagonist in vivo and in vitroImmunology Today, 1991
- Idiopathic Parkinson's disease, progressive supranuclear palsy and glutathione metabolism in the substantia nigra of patientsNeuroscience Letters, 1986
- Inhibition of NADH-linked oxidation in brain mitochondria by 1-methyl-4-phenyl-pyridine, a metabolite of the neurotoxin, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridineLife Sciences, 1985
- IV. Differences in the metabolism of MPTP in the rodent and primate parallel differences in sensitivity to its neurotoxic effectsLife Sciences, 1985