scispace - formally typeset
Open AccessJournal ArticleDOI

Temporal and Spatial Dynamics of Cerebral Immune Cell Accumulation in Stroke

Reads0
Chats0
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

read more

Citations
More filters
Book ChapterDOI

Neuroinflammation and immune regulation in ischemic stroke: identification of new pharmacological targets

TL;DR: There is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia acting more on the modulation of these later events than targeting of specific steps in the ischemic cascade.
Journal ArticleDOI

Acute cerebral ischemia and inflammation

TL;DR: The article reviews the recent literature on the role of the inflammatory response in ischemic stroke and some studies on the mechanisms of the development of inflammation in the isChemic brain as well as information on possible markers for predicting the severity of IS.
Journal ArticleDOI

Preconditioning increases brain resistance against acute brain injury via neuroinflammation modulation.

TL;DR: In this paper, the authors summarize the pathophysiology of acute brain injury and discuss the involved mechanisms of neuroinflammation in ABI, as well as existing experimental and clinical studies demonstrating the efficacy of preconditioning methods in various types of ABI by modulating neuro inflammation.
Journal ArticleDOI

Neutrophil dynamics and inflammaging in acute ischemic stroke: A transcriptomic review

TL;DR: In this paper , the authors discuss how neutrophil-specific gene expression patterns may contribute to poor treatment responses in stroke patients and discuss age-related transcriptional changes that may lead to poor clinical outcomes and greater susceptibility to cerebrovascular diseases.
References
More filters
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Related Papers (5)