Abstract
Abstract Perihematomal edema (PHE) occurs within hours after intracerebral hemorrhage (ICH), leading to secondary injury manifested by impaired blood-brain-barrier (BBB) integrity and adjacent tissue destruction. To dissect mechanisms underlying PHE formation, we profiled human and mouse perihematomal tissues and identified natural killer (NK) cells as a predominant immune cell subset that outnumbers other infiltrating immune cell types during early stage of ICH. Unbiased clustering of single cell transcriptional profiles revealed two major NK cell subsets in the brain following ICH that possess either high cytotoxicity or robust chemokine production features, which distinguish them from NK cells in the periphery. NK cells exacerbate BBB disruption and brain edema after ICH via cytotoxicity toward cerebral endothelial cells and recruitment of neutrophils that augment focal inflammation. Thus, brain-bounding NK cells acquire specific features that contribute to PHE formation and neurological deterioration following ICH.
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