The anti-inflammatory cytokine, interleukin (IL)-10, blocks the inhibatory effect of IL-1 beta on long term potentiation - a role for JNK
Item Type:Journal Article
Citation:Kelly ?, Lynch A. Vereker E, Nolan Y, Queenan P, Whittaker E, O' Neill LAJ, Lynch MA., The anti-inflammatory cytokine, interleukin (IL)-10, blocks the inhibatory effect of IL-1 beta on long term potentiation - a role for JNK, Journal of Biological Chemistry, 276, 49, 2001, 45564 - 45572
The anti-inflammatory cytokine, interleukin (IL)-10, blocks the inhibitory effect of IL-1 beta on long term potentiation. A role for JNK.pdf (published (publisher copy) peer-reviewed) 573.1Kb
Several effects of the proinflammatory cytokine, interleukin-1? (IL-1?), have been described in the central nervous system, and one area of the brain where marked changes have been reported is the hippocampus. Among these changes are an IL-1?-induced inhibition of long term potentiation (LTP) in perforant path-granule cell synapses and an attenuation of glutamate release in synaptosomes prepared from the hippocampus. Evidence suggests that, at least in circulating cells, the anti-inflammatory cytokine, IL-10, antagonizes certain effects of IL-1. We investigated the effect of IL-10 on IL-1?-induced inhibition of LTP and glutamate release. The evidence presented indicates that IL-1? stimulates the stress-activated protein kinase, c-Jun-activated protein kinase (JNK), and IL-1 receptor-associated kinase, which may explain its inhibitory effect on release and LTP, and that IL-10 reversed the IL-1?-induced stimulation of JNK activity and inhibition of release and LTP. We observed that IL-10 abrogated the stimulatory effect of IL-1? on superoxide dismutase activity and reactive oxygen species production, whereas the H2O2-induced inhibition of LTP was also blocked by IL-10. We present evidence that suggests that the action of IL-10 may be mediated by its ability to induce shedding of the IL-1 type I receptor.
Type of material:Journal Article
Series/Report no:Journal of Biological Chemistry
Availability:Full text available