Interleukin-1 mediates ischaemic brain injury via distinct actions on endothelial cells and cholinergic neurons.

ABSTRACT: The cytokine interleukin-1 (IL-1) is a key contributor to neuroinflammation and brain injury, yet mechanisms by which IL-1 triggers neuronal injury remain unknown. Here we induced conditional deletion of IL-1R1 in brain endothelial cells, neurons and blood cells to assess site-specific IL-1 actions in a model of cerebral ischaemia in mice. Tamoxifen treatment of IL-1R1 floxed (^fl/fl) mice crossed with mice expressing tamoxifen-inducible Cre-recombinase under the Slco1c1 promoter resulted in brain endothelium-specific deletion of IL-1R1 and a significant decrease in infarct size (29%), blood-brain barrier (BBB) breakdown (53%) and neurological deficit (40%) compared to vehicle-treated or control (IL-1R1^fl/fl) mice. Absence of brain endothelial IL-1 signalling improved

SUBMITTER: Wong R 

PROVIDER: S-EPMC6363965 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature