Neuronal injury induces the release of pro-interleukin-1beta from activated microglia in vitro.

Brain Research
Penglian WangDavid Brough

Abstract

Microglia activated after brain injury, are a major source of the pro-inflammatory cytokine interleukin-1 (IL-1), which is known to further exacerbate damage. However, the mechanisms that control IL-1 release in acute neuronal injury are unknown and the purpose of this study was to test the hypothesis that neuronal injury induces IL-1beta release from microglial cells. Here we report that lipopolysaccharide (LPS)-activated rat microglia co-cultured with healthy rat neurons express pro-IL-1beta, which in the absence of cell death accumulates in the cells. Treatment of co-cultures with the excitotoxin N-methyl-D-aspartate (NMDA) induced neuronal cell death leading to the appearance of pro-IL-1beta in the culture supernatant. This effect was reversed by the NMDA receptor antagonist MK-801, and was neuron-dependent, since NMDA had no effect on cell death or pro-IL-1beta release in mixed glial cell cultures. In addition, we show that pro-IL-1beta release from LPS-treated mixed glia or LPS-treated microglia is significantly reduced in the presence of conditioned medium from healthy co-cultures or neuronal cultures respectively. These results demonstrate that injured neurons promote the release of pro-IL-1beta from microglia, possibly...Continue Reading

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Citations

Mar 18, 2016·Molecular Neurobiology·José IglesiasGeorge E Barreto
Mar 31, 2015·Frontiers in Cellular Neuroscience·Karlijn J DoornAnne-Marie van Dam
May 9, 2009·American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons·H R BoumaT A Schuurs
Mar 25, 2021·Fluids and Barriers of the CNS·María Del Mar Fernández-ArjonaJesús M Grondona

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