Lipopolysaccharide-induced increase in signalling in hippocampus is abrogated by IL-10 - A role for IL-1β?

Aileen M. Lynch, Christine Walsh, Ada Delaney, Yvonne Nolan, Veronica A. Campbell, Marina A. Lynch

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112 Citations (Scopus)


Parenterally administered lipopolysaccharide (LPS) increases the concentration of the pro-inflammatory cytokine interleukin-1β (IL-1β) in the rat hippocampus and evidence suggests that this effect plays a significant role in inhibiting long-term potentiation (LTP). The anti-inflammatory cytokine IL-10, antagonizes certain effects of IL-1β, so if the effects of LPS are mediated through an increase in IL-1β, it might be predicted that IL-10 would also abrogate the effect of LPS. Here, we report that IL-10 reversed the inhibitory effect of LPS on LTP and the data couple this with an inhibitory effect on the LPS-induced increase in IL-1β. LPS treatment increased hippocampal expression of IL-1 receptor Type I protein. Consistent with the LPS-induced increases in IL-1β concentration and receptor expression, were downstream changes which included enhanced phosphorylation of IRAK and the stress-activated kinases, JNK and p38; these LPS-induced changes were reversed by IL-10, which concurs with the idea that these events are triggered by increased activation of IL-1RI by IL-1β. We provide evidence which indicates that LPS treatment leads to evidence of cell death and this was reversed in hippocampus prepared from LPS-treated rats which received IL-10. The evidence is therefore consistent with the idea that IL-10 acts to protect neuronal tissue from the detrimental effects induced by LPS.

Original languageEnglish
Pages (from-to)635-646
Number of pages12
JournalJournal of Neurochemistry
Issue number3
Publication statusPublished - Feb 2004
Externally publishedYes


  • Cell death
  • Hippocampus
  • IL-1β
  • IL-10
  • Lipopolysaccharide
  • Long-term potentiation


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