Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1) in a number of injury paradigms. Low concentrations of IL-1 potentiated hypoxia-induced neurodegeneration whilst high concentrations had no effect. In contrast, higher concentrations of IL-1 were strongly neuroprotective in models of combined oxygen/glucose deprivation and N-methyl-D-aspartate toxicity, but no potentiation was observed at low IL-1 concentrations. Both protective and toxic effects of IL-1 were fully antagonized by IL-1 receptor antagonist. These data demonstrate that the effects of IL-1 on neuronal injury are complex, and may be directly related to the injury paradigm studied
Interleukin-1b (IL-1b), a polypeptide immune mediator, is in-duced within the central nervous system...
Background: In Alzheimer's disease, stroke and brain injuries, activated microglia can release proin...
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervou...
Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1...
Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Interleukin (IL)-1 is a pivotal pro-inflammatory cytokine and an important mediator of both acute an...
Inflammation occurs rapidly in response to acute brain insults such as stroke, haemorrhage or trauma...
Abstract Perinatal hypoxia/ischemia (HI) is a common cause of neurological deficits in children. Int...
The inflammatory cytokines interleukin-1\u2424 and tumor necrosis factor-\u2423 (TNF-\u2423) have be...
An inadequate supply of oxygen in the brain may lead to an inflammatory response through neuronal an...
Interleukin-1 (IL-1) is one of the most important pro-inflammatory cytokines and plays a pivotal rol...
C1 - Journal Articles RefereedInterleukin (IL)-1beta plays an important role in the inflammatory res...
Interleukin-1b (IL-1b), a polypeptide immune mediator, is in-duced within the central nervous system...
Background: In Alzheimer's disease, stroke and brain injuries, activated microglia can release proin...
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervou...
Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1...
Using organotypic hippocampal slice cultures we have investigated the actions of Interleukin-1 (IL-1...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Changes in interleukin-β (IL-β) levels and/or signaling have been implicated in the pathogenesis of ...
Interleukin (IL)-1 is a pivotal pro-inflammatory cytokine and an important mediator of both acute an...
Inflammation occurs rapidly in response to acute brain insults such as stroke, haemorrhage or trauma...
Abstract Perinatal hypoxia/ischemia (HI) is a common cause of neurological deficits in children. Int...
The inflammatory cytokines interleukin-1\u2424 and tumor necrosis factor-\u2423 (TNF-\u2423) have be...
An inadequate supply of oxygen in the brain may lead to an inflammatory response through neuronal an...
Interleukin-1 (IL-1) is one of the most important pro-inflammatory cytokines and plays a pivotal rol...
C1 - Journal Articles RefereedInterleukin (IL)-1beta plays an important role in the inflammatory res...
Interleukin-1b (IL-1b), a polypeptide immune mediator, is in-duced within the central nervous system...
Background: In Alzheimer's disease, stroke and brain injuries, activated microglia can release proin...
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervou...