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Open AccessJournal ArticleDOI

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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HDAC Inhibitor Sodium Butyrate-Mediated Epigenetic Regulation Enhances Neuroprotective Function of Microglia During Ischemic Stroke

TL;DR: Evidence of HDAC inhibition being a promising molecular switch to epigenetically modify microglial behavior from pro-inflammatory to anti-inflammatory which could mitigate microglia-mediated neuroinflammation is shown.
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Danger signals in stroke and their role on microglia activation after ischemia

TL;DR: The role of the most important DAMPs, high mobility group box 1, heat and cold shock proteins, purines, and peroxiredoxins, are addressed and intracellular pathways activated by DAMPs in microglia are illuminated.
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Role of spleen-derived monocytes/macrophages in acute ischemic brain injury

TL;DR: The dissociative findings ofinfarct size and extent of MM infiltration in the postischemic brain indicate minimal involvement of spleen-derived total MMs in acute infarct development, and selective Ly-6Chigh or Ly- 6Clow MM targeting is suggested to address the contribution of the individual subset to acute stroke pathologic assessment.
Journal ArticleDOI

Mechanisms contributing to cerebral infarct size after stroke: gender, reperfusion, T lymphocytes, and Nox2-derived superoxide.

TL;DR: Evidence is provided in mice that gender difference in cerebral infarct volume only occurs when the ischemic brain is reperfused, and mechanisms that could be therapeutically targeted in acute isChemic stroke patients who receive thrombolysis therapy to induce cerebral reperfusion are provided.
Journal ArticleDOI

Peroxisome proliferator-activated receptor γ (PPARγ): A master gatekeeper in CNS injury and repair.

TL;DR: The therapeutic potential of PPARγ in stroke and brain trauma is reviewed and the novel role of PParγ in long-term tissue repair is highlighted, which lies at the apex of cell fate decisions and exerts profound effects on the chronic progression of acute injury conditions.
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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