Temporal and spatial dynamics of cerebral immune cell accumulation in stroke.

@article{Gelderblom2009TemporalAS,
  title={Temporal and spatial dynamics of cerebral immune cell accumulation in stroke.},
  author={Mathias Gelderblom and Frank Leypoldt and Karin Steinbach and D. Behrens and Chi-un Choe and Dominic A. Siler and Thiruma V. Arumugam and Ellen Orthey and Christian Gerloff and Eva Tolosa and Tim Magnus},
  journal={Stroke},
  year={2009},
  volume={40 5},
  pages={
          1849-57
        }
}
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… 
T‐cells and macrophages peak weeks after experimental stroke: Spatial and temporal characteristics
TLDR
The data show that T‐cells are present in higher numbers in the corpus callosum compared to the rest of the brain (except from the infarct core where they were highest), and that leukocyte infiltration at different time points after experimental stroke in mice is investigated.
Dissecting functional phenotypes of microglia and macrophages in the rat brain after transient cerebral ischemia
TLDR
It is proposed that BM‐macrophages recruited to the injured brain early after ischemia could contribute to functional recovery after stroke, but they switch toward a pro‐inflammatory phenotype in the ischemic parenchyma.
The Role of Immune Cells in Post-Stroke Angiogenesis and Neuronal Remodeling: The Known and the Unknown
TLDR
To better understand the multiple roles of immune cells in neural tissue repair processes post stroke, a comprehensive understanding of these inflammatory mechanisms may help identify potential targets for the development of novel immunoregulatory therapeutic strategies that ameliorate complications and improve functional rehabilitation after stroke.
CD38 Exacerbates Focal Cytokine Production, Postischemic Inflammation and Brain Injury after Focal Cerebral Ischemia
TLDR
CD38 is differentially regulated following stroke and its deficiency attenuates the postischemic chemokine production, the immune cell infiltration and the cerebral injury after temporary ischemia and reperfusion, and might prove a therapeutic target in ischemic stroke.
FGF21 alleviates neuroinflammation following ischemic stroke by modulating the temporal and spatial dynamics of microglia/macrophages
TLDR
RhFGF21 treatment promoted functional recovery in experimental stroke by modulating microglia/macrophage-mediated neuroinflammation via the NF-κB and PPAR-γ signaling pathways, making it a potential anti-inflammatory agent for stroke treatment.
CNS-border associated macrophages respond to acute ischemic stroke attracting granulocytes and promoting vascular leakage
TLDR
Findings show ischemia-induced reprogramming of the gene expression profile of CD163+ macrophages that has a rapid impact on leukocyte chemotaxis and blood-brain barrier integrity, and promotes neurological impairment in the acute phase of stroke.
Experimental Stroke Differentially Affects Discrete Subpopulations of Splenic Macrophages
TLDR
The findings suggest that selective splenic macrophage functions could be impaired after stroke and the contribution of macrophages to stroke-associated pathology and infectious complications should be considered at a subset-specific level.
Quantitative and Correlational Analysis of Brain and Spleen Immune Cellular Responses Following Cerebral Ischemia
TLDR
The correlation among neurological deficit and various immune cells suggests that microglia and splenic adaptive immune cells are protective while infiltrating peripheral myeloid cells (macrophage and neutrophils) worsen stroke outcome.
Sterile Inflammation after Permanent Distal MCA Occlusion in Hypertensive Rats
TLDR
This study delineates the sequence of cellular inflammation after stroke in spontaneously hypertensive (SH) rats and validates this strain for further translational research in poststroke inflammation.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 50 REFERENCES
Role of T Lymphocytes and Interferon-γ in Ischemic Stroke
TLDR
Findings indicate that CD4+ and CD8+ T lymphocytes, but not B lymphocyte, contribute to the inflammatory and thrombogenic responses, brain injury, and neurological deficit associated with experimental stroke.
Role of T lymphocytes and interferon-gamma in ischemic stroke.
TLDR
It is indicated that CD4+ and CD8+ T lymphocytes, but not B lymphocyte, contribute to the inflammatory and thrombogenic responses, brain injury, and neurological deficit associated with experimental stroke.
Reperfusion following focal stroke hastens inflammation and resolution of ischemic injured tissue
TLDR
Changes which occur after Temporary Middle Cerebral Artery Occlusion (TMCAO; 80 or 160 min) followed by reperfusion are characterized and compared these changes to those which occur following PMCAO.
Flow Cytometric Analysis of Inflammatory Cells in Ischemic Rat Brain
TLDR
Quantitative flow cytometric analysis of ischemic rat brain is feasible and provides a reliable and rapid assay to assess neuroinflammation in experimental models of brain ischemia.
Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke.
TLDR
An important role is suggested for ICAM-1-mediated PMN adhesion in the pathophysiology of evolving stroke and wild-type mice subjected to 45 min of ischemia followed by 22 h of reperfusion are suggested.
...
1
2
3
4
5
...