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Published on: June 11, 2019
Cord blood rescues stroke-induced changes in splenocyte phenotype and function
Martina Vendrame1, Carmelina Gemma, Keith R Pennypacker
1Center for Excellence in Aging and Brain Repair, MDC 78, University of South Florida College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA.
Human umbilical cord blood cells (HUCBC) protect against stroke by modulating the immune response. HUCBC treatment reduced spleen damage and brain injury in a rat stroke model, suggesting a novel immunomodulatory mechanism.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Stroke induces significant immuno-inflammatory responses.
- The neuroprotective mechanisms of human umbilical cord blood cells (HUCBC) in stroke models are not fully understood.
- HUCBC are known to migrate to injured tissues, including potentially the spleen following stroke.
Purpose of the Study:
- To investigate the immunomodulatory effects of HUCBC in a rat middle cerebral artery occlusion (MCAO) stroke model.
- To determine if HUCBC-mediated protection is linked to the modulation of splenic immune responses.
- To explore the impact of HUCBC on T-cell populations and cytokine production post-stroke.
Main Methods:
- Induction of MCAO in rats to create a stroke model.
- Administration of HUCBC treatment following MCAO.
- Assessment of spleen weight, splenic CD8+ T-cell counts, and brain injury extent.
- Splenocyte proliferation assays to analyze cytokine production (IL-10 and IFN-gamma).
Main Results:
- MCAO caused spleen size reduction and decreased CD8+ T-cell counts, correlating with ischemic damage.
- HUCBC treatment reversed spleen size reduction and restored CD8+ T-cell counts.
- HUCBC treatment significantly reduced brain injury in MCAO rats.
- HUCBC treatment modulated T-cell responses by increasing IL-10 and decreasing IFN-gamma production.
Conclusions:
- HUCBC exhibit neuroprotective effects in the rat MCAO stroke model.
- HUCBC mediate protection through an immunomodulatory mechanism involving spleen and T-cell responses.
- This study suggests a novel role for HUCBC in regulating post-stroke inflammation.
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