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Title: The anti-inflammatory cytokine, interleukin (IL)-10, blocks the inhibatory effect of IL-1 beta on long term potentiation - a role for JNK
Sponsor: Health Research Board
Enterprise Ireland
Higher Education Authority
European Union (EU)
Author's Homepage:
Keywords: Physiology
Issue Date: 2001
Publisher: American Society for Biochemistry and Molecular Biology
Citation: Áine Kelly, Aileen Lynch, Emily Vereker, Yvonne Nolan, Patrice Queenan, Elizabeth Whittaker, Luke A. J. O' Neill, and Marina A. Lynch ‘The anti-inflammatory cytokine, interleukin (IL)-10, blocks the inhibatory effect of IL-1 beta on long term potentiation - a role for JNK’ in Journal of Biological Chemistry, 276, (49), 2001, pp 45564 - 45572
Series/Report no.: Journal of Biological Chemistry
Abstract: Several effects of the proinflammatory cytokine, interleukin-1β (IL-1β), 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-1β-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-1β-induced inhibition of LTP and glutamate release. The evidence presented indicates that IL-1β 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-1β-induced stimulation of JNK activity and inhibition of release and LTP. We observed that IL-10 abrogated the stimulatory effect of IL-1β 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.
Description: PUBLISHED
Appears in Collections:Physiology (Scholarly Publications)

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