A transient decrease in spleen size following stroke corresponds to splenocyte release into systemic circulation

Hilary A. Seifert; Aaron A. Hall; Cortney B. Chapman; Lisa A. Collier; Alison E. Willing; Keith R. Pennypacker

doi:10.1007/s11481-012-9406-8

A transient decrease in spleen size following stroke corresponds to splenocyte release into systemic circulation

Hilary A. Seifert, Aaron A. Hall, Cortney B. Chapman, Lisa A. Collier, Alison E. Willing, Keith R. Pennypacker

Research output: Contribution to journal › Review article › peer-review

145 Scopus citations

Abstract

The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.

Original language	English
Pages (from-to)	1017-1024
Number of pages	8
Journal	Journal of NeuroImmune Pharmacology
Volume	7
Issue number	4
DOIs	https://doi.org/10.1007/s11481-012-9406-8
State	Published - Dec 2012

Bibliographical note

Funding Information:
Acknowledgements The authors would like to thank the Lisa Muma Weitz Laboratory for Advanced Microscopy & Cell Imaging for their assistance with acquiring the confocal microscopy images. This study was funded by the National Institutes of Health grant RO1 NS052839.

Keywords

Brain ischemia
MCAO
Monocytes
Natural killer cells
T cells

ASJC Scopus subject areas

Neuroscience (miscellaneous)
Immunology and Allergy
Immunology
Pharmacology

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10.1007/s11481-012-9406-8

Cite this

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title = "A transient decrease in spleen size following stroke corresponds to splenocyte release into systemic circulation",

abstract = "The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.",

keywords = "Brain ischemia, MCAO, Monocytes, Natural killer cells, T cells",

author = "Seifert, {Hilary A.} and Hall, {Aaron A.} and Chapman, {Cortney B.} and Collier, {Lisa A.} and Willing, {Alison E.} and Pennypacker, {Keith R.}",

note = "Funding Information: Acknowledgements The authors would like to thank the Lisa Muma Weitz Laboratory for Advanced Microscopy & Cell Imaging for their assistance with acquiring the confocal microscopy images. This study was funded by the National Institutes of Health grant RO1 NS052839.",

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AU - Seifert, Hilary A.

AU - Hall, Aaron A.

AU - Chapman, Cortney B.

AU - Collier, Lisa A.

AU - Willing, Alison E.

AU - Pennypacker, Keith R.

N1 - Funding Information: Acknowledgements The authors would like to thank the Lisa Muma Weitz Laboratory for Advanced Microscopy & Cell Imaging for their assistance with acquiring the confocal microscopy images. This study was funded by the National Institutes of Health grant RO1 NS052839.

PY - 2012/12

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N2 - The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.

AB - The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.

KW - Brain ischemia

KW - MCAO

KW - Monocytes

KW - Natural killer cells

KW - T cells

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JF - Journal of NeuroImmune Pharmacology

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ER -

A transient decrease in spleen size following stroke corresponds to splenocyte release into systemic circulation

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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