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Hypothermia reduces toll-like receptor 3-activated microglial interferon-β and nitric oxide production

Tomohiro Matsui1, Yukari Motoki, Yusuke Yoshida

  • 1Department of Laboratory Sciences, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-kogushi, Ube, Yamaguchi 755-8505, Japan.

Mediators of Inflammation
|April 17, 2013
PubMed

Insights

Therapeutic hypothermia reduces harmful microglial responses after central nervous system (CNS) injury. This neuroprotective effect is linked to decreased production of interferon-beta and nitric oxide by microglia.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Therapeutic hypothermia is a neuroprotective strategy following central nervous system (CNS) injury.
  • Microglia, the resident immune cells of the CNS, express toll-like receptors (TLRs) and contribute to sterile CNS injury pathogenesis.
  • Interferon-beta (IFN-β) and nitric oxide (NO) released by activated microglia are implicated in neuronal cell death.

Purpose of the Study:

  • To investigate the mechanisms underlying the neuroprotective effects of therapeutic hypothermia.
  • To examine the impact of hypothermic culture conditions on TLR3-activated microglial production of IFN-β and NO.
  • To determine if reduced IFN-β and NO contribute to hypothermia-mediated neuroprotection.

Main Methods:

  • Primary rat and mouse microglia were cultured under hypothermic (33°C) and normothermic (37°C) conditions.
  • Microglia were activated using polyinosinic-polycytidylic acid, a TLR3 agonist.
  • Production of IFN-β and NO was measured at 48 hours.
  • Neuronal cell death was assessed after exposure to recombinant IFN-β and a NO donor (sodium nitroprusside).

Main Results:

  • Hypothermic culture significantly decreased the production of IFN-β and NO in TLR3-activated microglia compared to normothermic culture.
  • Exposure to IFN-β and NO induced concentration-dependent death in rat neuronal PC12 cells.
  • These findings indicate a direct link between microglial mediators and neuronal viability.

Conclusions:

  • Therapeutic hypothermia attenuates the release of IFN-β and NO from activated microglia.
  • This reduction in pro-inflammatory mediators by hypothermia contributes to the inhibition of neuronal cell death.
  • The study elucidates a key mechanism for hypothermia's neuroprotective role in CNS injury.

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