The neuroprotective mechanism of human umbilical cord blood cells (HUCBC) in the rat middle cerebral artery occlusion (MCAO) stroke model remains uncertain. Given the inflammatory sequelae that occur following stroke, we investigated whether HUCBC protection could be derived from the modulation of this immuno-inflammatory event, suggested by the attraction of the HUCBC to the spleen. We found that, following MCAO, rat spleen size was reduced concomitantly with their CD8+ T-cell counts. Interestingly, MCAO-induced spleen size reduction correlated with the extent of ischemic damage, however, HUCBC treatment rescued the spleen weight, splenic CD8+ T-cell counts, as well as the amount of brain injury. Additionally, splenocyte proliferation assays demonstrated that HUCBC treatment opposed MCAO-associated T-cell proliferation by increasing the production of IL-10 while decreasing IFN-γ. Taken together, these results suggest a novel immunomodulatory mechanism by which HUCBC mediate protection in the rat MCAO model of stroke.
|Number of pages||10|
|State||Published - May 2006|
Bibliographical noteFunding Information:
This work was supported by the American Heart Association (#0355183B, AEW) and Saneron CCEL Therapeutics, who provided the HUCBC. PRS is co-founder, and AW and PCB are consultants of Saneron CCEL Therapeutics, Inc. AEW and PRS are inventors on HUCBC patent applications.
Copyright 2008 Elsevier B.V., All rights reserved.
ASJC Scopus subject areas
- Developmental Neuroscience