Extent of ischemic brain injury following thrombotic stroke is independent of the NLRP3 inflammasome

Eloise Lemarchand, Jack Barrington, Alistair Chenery, Michael Haley, Graham Coutts, Judith Allen, Stuart Allan, David Brough

Research output: Contribution to journalArticlepeer-review


Background and Purpose - A major process contributing to cell death in the ischemic brain is inflammation. Inflammasomes are multi-molecular protein complexes that drive inflammation through activation of pro-inflammatory cytokines such as interleukin (IL)-1β. Pre-clinical evidence suggests that IL-1β contributes to a worsening of ischemic brain injury.
Methods - Using a mouse middle cerebral artery thrombosis model we examined the inflammatory response after stroke, and the contribution of the NLRP3 inflammasome to ischemic injury.
Results - There was a marked inflammatory response after stroke characterised by increased expression of pro-inflammatory cytokines and NLRP3, and by recruitment of leukocytes to the injured tissue. Targeting NLRP3 with the inhibitor MCC950, or using mice in which NLRP3 was knocked out, had no effect on the extent of injury caused by stroke.
Conclusions - These data suggest that the NLRP3 pathway does not contribute to the inflammation exacerbating ischemic brain damage, contradicting several recent reports to the contrary.
Original languageEnglish
Early online date8 Apr 2019
Publication statusPublished - 2019


  • NLRP3 inflammasome
  • inflammation
  • cerebral ischemia
  • cytokine, IL-1

Research Beacons, Institutes and Platforms

  • Lydia Becker Institute


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