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Stereological and Flow Cytometry Characterization of Leukocyte Subpopulations in Models of Transient or Permanent Cerebral Ischemia
Published on: December 28, 2014
Expression of interleukin-17 in ischemic brain tissue.
1Department of Neurology, the First Affiliated Clinic College of Harbin Medical University, Harbin, China.
Scandinavian Journal of Immunology
|November 25, 2005
Summary
Interleukin-17 (IL-17) is elevated in human and rat brains after ischemic injury, indicating its role in brain inflammation. Neuroglial cells, not just T cells, may produce IL-17 during ischemic events.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Ischemic brain injury triggers acute inflammation and cytokine accumulation.
- Cytokines are crucial for leukocyte recruitment and inflammatory processes in brain injury.
- Interleukin-17 (IL-17) is a recently identified cytokine linked to T-cell activity.
Purpose of the Study:
- To investigate the source and action of IL-17 in cerebral ischemia.
- To compare IL-17 expression in human and rat ischemic brain models.
- To determine the cellular origin of IL-17 in brain ischemia.
Main Methods:
- Immunohistochemistry to assay IL-17 levels in human brain tissue.
- Permanent middle cerebral artery occlusion (pMCAO) in Sprague-Dawley rats.
- In situ hybridization for IL-17 mRNA expression in rats.
- Double-staining for IL-17 and glial fibrillary acidic protein (GFAP) in rat neuroglial cells.
Main Results:
- IL-17 levels were elevated in human ischemic brain hemispheres, peaking at days 3-5 post-ischemia.
- IL-17 mRNA expression increased in rat ischemic hemispheres, peaking around day 6.
- Extensive co-localization of IL-17 and GFAP was observed in rat ischemic hemispheres, suggesting neuroglial cell production.
Conclusions:
- IL-17 is involved in the inflammatory response to human brain ischemia.
- Neuroglial cells are a significant source of IL-17 in the later stages of ischemic brain injury in rats.
- Findings suggest neuroglial cells, in addition to T cells, contribute to IL-17 production during brain ischemia.
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