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Temporal and Spatial Dynamics of Cerebral Immune Cell Accumulation in Stroke

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TLDR
The peculiar activation pattern and massive increase of antigen-presenting cells in temporal conjunction with regulatory cells might provide additional insight into poststroke immune regulation.
Abstract
Background and Purpose— Ischemic stroke leads to significant morbidity and mortality in the Western world Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage The understanding of postischemic inflammation is very limited The objectives of this study were to define the temporal and spatial infiltration of immune cell populations and their activation patterns in a murine cerebral ischemia–reperfusion injury model Methods— Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice Immunohistochemistry and flow cytometry were used to quantify the infiltrating immune cell subsets Results— Accumulation of microglia and infiltration of the ischemic hemisphere by macrophages, lymphocytes, and dendritic cells (DCs) preceded the neutrophilic influx DCs were found to increase 20-fold and constituted a substantial proportion of infiltrating cells DCs exhi

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Endogenous recovery after brain damage: molecular mechanisms that balance neuronal life/death fate.

TL;DR: This review summarizes a handful of endogenously activated mechanisms that balance molecular cues so as to determine whether neurons recover from injury or die and emphasizes the need to construct integrated models of neuronal degeneration and survival that converge in neuronal fate after injury.
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Multiplex immunoassay characterization and species comparison of inflammation in acute and non-acute ischemic infarcts in human and mouse brain tissue

TL;DR: Results reveal how the chronic inflammatory response to stroke is impacted by age, sex, and multiple strokes in mice, and correlation and two-way ANOVA analyses reveal that despite this substantial overlap between species, there are still significant differences, particularly in the regulation of granulocyte colony-stimulating factor, which is increased in mice but not in humans.
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Pretreatment Cancer-Related Cognitive Impairment-Mechanisms and Outlook.

TL;DR: The state of the science of CRCI independent of treatment is summarized and the ability of peripheral tumors to alter CNS pathways in murine models is compelling, and it allows researchers to isolate the underlying biological mechanisms from the confounding psychosocial stressors found in the clinic.
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Neuroinflammatory responses in experimental and human stroke lesions

TL;DR: It is revealed that despite similarities in the core signature of the inflammatory reaction, human stroke lacks clearly definable temporal and spatial sequences of lesion maturation that can be generalized and applied for a large patient population and precise and stage-dependent targeting of neuroinflammation in human stroke patients will be difficult to achieve.
References
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Journal ArticleDOI

Pathobiology of ischaemic stroke: an integrated view

TL;DR: This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
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Microglia: active sensor and versatile effector cells in the normal and pathologic brain

TL;DR: This review focuses on several key observations that illustrate the multi-faceted activities of microglia in the normal and pathologic brain.
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Taking dendritic cells into medicine

TL;DR: Some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy are presented.
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The inflammatory response in stroke.

TL;DR: The role of specific cell types including leukocytes, endothelium, glia, microglia, the extracellular matrix and neurons, and mediators produced by inflammatory cells such as cytokines, chemokines, reactive oxygen species and arachidonic acid metabolites are reviewed.
Journal ArticleDOI

A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells.

TL;DR: A synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14+) is preventive against EAE and targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.
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