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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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Citations
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Journal ArticleDOI

Pathophysiology, treatment, and animal and cellular models of human ischemic stroke

TL;DR: This review explores the etiology and pathogenesis of ischemic stroke, and provides a general model of such, and explores new and emerging approaches for the prevention and treatment of stroke.
Journal ArticleDOI

The biphasic function of microglia in ischemic stroke.

TL;DR: The mechanisms involved in regulating microglia activation and polarization were reviewed and the role of microRNAs and transplanted stem cells in mediating microgliancation and polarization during brain ischemia was studied.
Journal ArticleDOI

Inflammation in intracerebral hemorrhage: from mechanisms to clinical translation.

TL;DR: This review summarizes recent progress concerning the mechanisms underlying ICH-induced inflammation, and focuses on the inflammatory signaling pathways involved in microglial activation and TLR signaling, and explores potential therapeutic interventions by targeting the removal of hematoma components and inhibition ofTLR signaling.
Journal ArticleDOI

The role of peripheral immune cells in the CNS in steady state and disease

TL;DR: Strategies for targeting peripheral immune cells to reduce CNS disease burden are assessed on the basis of observations of myeloid cells in the CNS parenchyma and at CNS–periphery interfaces.
Journal ArticleDOI

Temporal pattern of expression and colocalization of microglia/macrophage phenotype markers following brain ischemic injury in mice

TL;DR: These data show that the ischemic lesion is accompanied by activation of specific microglia/macrophage phenotype that presents distinctive spatial and temporal features that provide a basis for understanding this complex response and for developing strategies resulting in promotion of a protective inflammatory phenotype.
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.
Journal ArticleDOI

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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