IL-17 potentiates neuronal injury induced by oxygen-glucose deprivation and affects neuronal IL-17 receptor expression

J Neuroimmunol. 2009 Jul 25;212(1-2):17-25. doi: 10.1016/j.jneuroim.2009.04.007. Epub 2009 May 19.

Abstract

Interleukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry. In the in vitro model of oxygen-glucose deprivation (OGD), IL-17 showed a dose-dependent effect in promoting neuronal injury through IL-17-IL-17R combination which can be blocked by IL-17R/Fc chimera. Our results demonstrated the up-regulation of IL-17 and IL-17R following permanent middle cerebral artery occlusion and suggested that they contributed to stroke outcome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Brain Ischemia / pathology*
  • Cell Hypoxia*
  • Cells, Cultured
  • Glucose / metabolism*
  • Hippocampus / pathology
  • Humans
  • Interleukin-17 / analysis
  • Interleukin-17 / genetics
  • Interleukin-17 / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neurons / pathology*
  • Receptors, Interleukin-17 / analysis
  • Receptors, Interleukin-17 / genetics
  • Receptors, Interleukin-17 / physiology*

Substances

  • Interleukin-17
  • Receptors, Interleukin-17
  • Glucose