Cord blood rescues stroke-induced changes in splenocyte phenotype and function

Martina Vendrame; Carmelina Gemma; Keith R. Pennypacker; Paula C. Bickford; Cyndy Davis Sanberg; Paul R. Sanberg; Alison E. Willing

doi:10.1016/j.expneurol.2006.03.017

Cord blood rescues stroke-induced changes in splenocyte phenotype and function

Martina Vendrame
, Carmelina Gemma
, Keith R. Pennypacker
, Paula C. Bickford
, Cyndy Davis Sanberg
, Paul R. Sanberg
, Alison E. Willing

Research output: Contribution to journal › Article › peer-review

221 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	191-200
Number of pages	10
Journal	Experimental Neurology
Volume	199
Issue number	1
DOIs	https://doi.org/10.1016/j.expneurol.2006.03.017
State	Published - May 2006

Bibliographical note

Funding 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:
Copyright 2008 Elsevier B.V., All rights reserved.

Funding

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.

Funders	Funder number
HUCBC
Saneron CCEL Therapeutics Inc.
American the American Heart Association	0355183B
American the American Heart Association

ASJC Scopus subject areas

Neurology
Developmental Neuroscience

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10.1016/j.expneurol.2006.03.017

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title = "Cord blood rescues stroke-induced changes in splenocyte phenotype and function",

abstract = "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.",

author = "Martina Vendrame and Carmelina Gemma and Pennypacker, \{Keith R.\} and Bickford, \{Paula C.\} and \{Davis Sanberg\}, Cyndy and Sanberg, \{Paul R.\} and Willing, \{Alison E.\}",

note = "Funding 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: Copyright 2008 Elsevier B.V., All rights reserved.",

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AU - Vendrame, Martina

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AU - Bickford, Paula C.

AU - Davis Sanberg, Cyndy

AU - Sanberg, Paul R.

AU - Willing, Alison E.

N1 - Funding 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: Copyright 2008 Elsevier B.V., All rights reserved.

PY - 2006/5

Y1 - 2006/5

N2 - 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.

AB - 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.

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Cord blood rescues stroke-induced changes in splenocyte phenotype and function

Abstract

Bibliographical note

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ASJC Scopus subject areas

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