The splenic response to stroke: From rodents to stroke subjects

Hilary A. Seifert, Halina Offner

Research output: Contribution to journalReview article

8 Citations (Scopus)

Abstract

Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke. Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.

Original languageEnglish (US)
Article number195
JournalJournal of Neuroinflammation
Volume15
Issue number1
DOIs
StatePublished - Jul 3 2018

Fingerprint

Rodentia
Stroke
Spleen
Cause of Death
Animal Models
Splenectomy
Outcome Assessment (Health Care)

Keywords

  • Animal models
  • Clinical studies
  • Immune response
  • Splenectomy
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience

Cite this

The splenic response to stroke : From rodents to stroke subjects. / Seifert, Hilary A.; Offner, Halina.

In: Journal of Neuroinflammation, Vol. 15, No. 1, 195, 03.07.2018.

Research output: Contribution to journalReview article

@article{f3282433714c44e1ae18949ceab291d0,
title = "The splenic response to stroke: From rodents to stroke subjects",
abstract = "Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke. Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.",
keywords = "Animal models, Clinical studies, Immune response, Splenectomy, Stroke",
author = "Seifert, {Hilary A.} and Halina Offner",
year = "2018",
month = "7",
day = "3",
doi = "10.1186/s12974-018-1239-9",
language = "English (US)",
volume = "15",
journal = "Journal of Neuroinflammation",
issn = "1742-2094",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - The splenic response to stroke

T2 - From rodents to stroke subjects

AU - Seifert, Hilary A.

AU - Offner, Halina

PY - 2018/7/3

Y1 - 2018/7/3

N2 - Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke. Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.

AB - Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke. Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.

KW - Animal models

KW - Clinical studies

KW - Immune response

KW - Splenectomy

KW - Stroke

UR - http://www.scopus.com/inward/record.url?scp=85049422020&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85049422020&partnerID=8YFLogxK

U2 - 10.1186/s12974-018-1239-9

DO - 10.1186/s12974-018-1239-9

M3 - Review article

C2 - 29970193

AN - SCOPUS:85049422020

VL - 15

JO - Journal of Neuroinflammation

JF - Journal of Neuroinflammation

SN - 1742-2094

IS - 1

M1 - 195

ER -