Abstract
Spontaneous intracerebral hemorrhage (ICH) is a particularly severe type of stroke for which no specific treatment has been established yet. Although preclinical models of ICH have substantial methodological limitations, important insight into the pathophysiology has been gained. Mounting evidence suggests an important contribution of inflammatory mechanisms to brain damage and potential repair. Neuroinflammation evoked by intracerebral blood involves the activation of resident microglia, the infiltration of systemic immune cells and the production of cytokines, chemokines, extracellular proteases and reactive oxygen species (ROS). Previous studies focused on innate immunity including microglia, monocytes and granulocytes. More recently, the role of adaptive immune cells has received increasing attention. Little is currently known about the interactions among different immune cell populations in the setting of ICH. Nevertheless, immunomodulatory strategies are already being explored in ICH. To improve the chances of translation from preclinical models to patients, a better characterization of the neuroinflammation in patients is desirable.
Highlights
Intracerebral hemorrhages (ICH) account for 10–15% of all strokes (Qureshi et al, 2009)
Neuroinflammation evoked by intracerebral blood involves the activation of resident microglia, the infiltration of systemic immune cells and the production of cytokines, chemokines, extracellular proteases and reactive oxygen species (ROS)
We found that CD4+ T cells are the predominating brain infiltrating leukocyte population in mice already 1 day after intracerebral hemorrhage (ICH) and their number peaked at day 5 (Mracsko et al, 2014)
Summary
Reviewed by: Vikramjeet Singh, Ludwig Maximilian University of Munich, Germany Halina Offner, Oregon Health and Science University, USA. Spontaneous intracerebral hemorrhage (ICH) is a severe type of stroke for which no specific treatment has been established yet. Preclinical models of ICH have substantial methodological limitations, important insight into the pathophysiology has been gained. Neuroinflammation evoked by intracerebral blood involves the activation of resident microglia, the infiltration of systemic immune cells and the production of cytokines, chemokines, extracellular proteases and reactive oxygen species (ROS). Previous studies focused on innate immunity including microglia, monocytes and granulocytes. The role of adaptive immune cells has received increasing attention. Little is currently known about the interactions among different immune cell populations in the setting of ICH. To improve the chances of translation from preclinical models to patients, a better characterization of the neuroinflammation in patients is desirable
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