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Inflammatory cell recruitment after experimental thromboembolic stroke in rats
- Source :
- Neuroscience. 279:139-154
- Publication Year :
- 2014
- Publisher :
- Elsevier BV, 2014.
-
Abstract
- Inflammatory mechanisms were recently identified as contributors to delayed neuronal damage after ischemic stroke. However, therapeutic strategies are still lacking, probably related to the outstanding standardization on inflammatory cell recruitment emerging from predominantly artificial stroke models, and the uncertainty on functional properties of distinct subpopulations. Using a rodent model of stroke that closely reflects human embolic ischemia, this study was focused on the local recruitment of immunoreactive cells as well as their functional and regional characterization. Wistar rats underwent thromboembolic middle cerebral artery occlusion, followed by intravenous injection of the blood-brain barrier permeability marker fluorescein-conjugated albumin at 24h. One hour later, brain tissue was subjected to multi-parameter flow cytometry and Pappenheim staining to characterize cells invaded into the ischemia-affected hemisphere, compared to the contralateral side. Immunofluorescence labeling was applied to explore the distribution patterns of recruited cells and their spatial relationships with the vasculature. One day after ischemia onset, a 6.12-fold increase of neutrophils and a 5.43-fold increase of monocytes/macrophages was found in affected hemispheres, while these cells exhibited enhanced major histocompatibility complex class II expression and allocation with vessels exhibiting impaired blood-brain barrier integrity. Microglia remained numerically unaltered in ischemic hemispheres, but shifted to an activated phenotype indicated by CD45/CD86 expression and morphological changes toward an ameboid appearance in the bordering zone. Ischemia caused an increase of lymphoid cells in close vicinity to the affected vasculature, while further analyses allowed separation into natural killer cells, natural killer T cells, T cells (added by an unconventional CD11b(+)/CD3(+) population) and two subpopulations of B cells. Taken together, our study provides novel data on the local inflammatory response to experimental thromboembolic stroke. As concomitantly present neutrophils, monocytes/macrophages and lymphoid cells in the early stage after ischemia induction correspond to changes seen in human stroke, future stroke research should preferably use animal models with relevance for clinical translation.
- Subjects :
- Male
Pathology
medicine.medical_specialty
Neutrophils
T-Lymphocytes
Population
Ischemia
Inflammation
Thromboembolic stroke
Monocytes
Brain Ischemia
Capillary Permeability
Random Allocation
cellular recruitment
Thromboembolism
medicine
Animals
Rats, Wistar
education
Stroke
CD86
B-Lymphocytes
education.field_of_study
Microglia
business.industry
Macrophages
General Neuroscience
Brain
Infarction, Middle Cerebral Artery
Natural killer T cell
medicine.disease
thromboembolic model
Killer Cells, Natural
Disease Models, Animal
medicine.anatomical_structure
inflammation
Blood-Brain Barrier
Immunology
medicine.symptom
business
Subjects
Details
- ISSN :
- 03064522
- Volume :
- 279
- Database :
- OpenAIRE
- Journal :
- Neuroscience
- Accession number :
- edsair.doi.dedup.....b9dc2b01f483f2b4486914ca6f6cf4fb