Intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke and carries high risk of mortality and disability.1 Although ICH causes primary brain damage from mass effect and disruption of brain parenchyma, the secondary injury from neuroinflammation plays a significant role in ICH pathogenesis.2 Toxicity due to extravasated blood components leads to the activation of microglia (residential immune cells in the CNS and astrocytes), infiltration of circulating immune cells including macrophages and T cells, and, subsequently, to the release of inflammatory cytokines, chemokines, free radicals, and other potentially toxic chemicals.3 This inflammatory response contributes to perihematomal edema (PHE) formation through increased blood-brain barrier (BBB) permeability surrounding the hematoma, which in turn, in a vicious cycle, exacerbates mass effect and augments apoptosis and recruitment of systemic leukocytes (including innate and adaptive immune cells) that eventually produces additional brain tissue inflammatory-related injury.2 Identification and characterization of the neuroimmune interactions involved in PHE formation may allow not only better understanding of pathophysiology of ICH but also could have significant clinical implications in the development of reliable biomarkers and targeted therapies.
