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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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Recombinant tissue plasminogen activator enhances microglial cell recruitment after stroke in mice.

TL;DR: It is reported for the first time that rtPA amplified microglia recruitment early after stroke in association with a rapid CCL3 production, which may take part in the higher susceptibility of rTPA-treated animals to reperfusion injury.
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Prospects and limitations of using endogenous neural stem cells for brain regeneration.

TL;DR: The endogenous NSCs are activated in response to disease or trauma, and produce new neurons and glia, suggesting they have the potential to regenerate damaged brain tissue while avoiding the above-mentioned problems.
Journal ArticleDOI

Inhibiting the Migration of M1 Microglia at Hyperacute Period Could Improve Outcome of tMCAO Rats.

TL;DR: To study whether inhibiting microglia migration to the ischemic boundary zone (IBZ) at the early phase could improve neurological outcomes after stroke, a large number of mice were fitted with EMTs to treat central giant cell granuloma.
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The Neuroprotective Effect of Genetic Mannose-binding Lectin Deficiency is not Sustained in the Sub-acute Phase of Stroke

TL;DR: Development of a successful anti-complement neuroprotective strategy will require carefully tailored inhibition coupled with a greater understanding of the functional effects of complement activation during later phases of stroke recovery.
Journal Article

Abstract WP277: Non-invasive Tracking of CD4+ T Cells With a Paramagnetic and Fluorescent Nanoparticle in Brain Ischemia

TL;DR: The use of MIRB coupled with in vivo imaging as a valid method to track CD4+ T cells in ischemic brain injury is demonstrated and will facilitate future investigations to identify the dynamics and key spatiotemporal events for brain-infiltrating lymphocytes in CNS inflammatory diseases.
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.
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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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