Role of Interleukin-10 in Acute Brain Injuries

Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 i...

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Published inFrontiers in neurology Vol. 8; p. 244
Main Authors Garcia, Joshua M., Stillings, Stephanie A., Leclerc, Jenna L., Phillips, Harrison, Edwards, Nancy J., Robicsek, Steven A., Hoh, Brian L., Blackburn, Spiros, Doré, Sylvain
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 12.06.2017
Subjects
concussion
endothelium
intracerebral hemorrhage
ischemia
Neuroscience
stroke
subarachnoid hemorrhage
intracerebral hemorrhage
endothelium
vasculature
subarachnoid hemorrhage
traumatic brain injury
concussion
stroke
ischemia
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Abstract Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. and models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
AbstractList Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. and models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
Author Robicsek, Steven A.
Blackburn, Spiros
Hoh, Brian L.
Edwards, Nancy J.
Doré, Sylvain
Garcia, Joshua M.
Leclerc, Jenna L.
Phillips, Harrison
Stillings, Stephanie A.
AuthorAffiliation 2 Department of Anesthesiology, College of Medicine, Center for Translational Research in Neurodegenerative Disease, University of Florida , Gainesville, FL , United States
7 Department of Neurosurgery, University of Florida , Gainesville, FL , United States
13 Department of Pharmaceutics, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
6 Department of Neurosurgery, University of California , San Francisco, CA , United States
12 Department of Psychiatry, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
8 Department of Neuroscience, University of Florida , Gainesville, FL , United States
9 Department of Neurosurgery, University of Texas , Houston, TX , United States
5 Department of Neurology, University of California , San Francisco, CA , United States
3 Department of Neuroscience, College of Medicine,
AuthorAffiliation_xml – name: 13 Department of Pharmaceutics, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
– name: 8 Department of Neuroscience, University of Florida , Gainesville, FL , United States
– name: 9 Department of Neurosurgery, University of Texas , Houston, TX , United States
– name: 10 Department of Neurology, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
– name: 1 College of Medicine, University of Florida , Gainesville, FL , United States
– name: 7 Department of Neurosurgery, University of Florida , Gainesville, FL , United States
– name: 12 Department of Psychiatry, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
– name: 2 Department of Anesthesiology, College of Medicine, Center for Translational Research in Neurodegenerative Disease, University of Florida , Gainesville, FL , United States
– name: 11 Department of Psychology, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida , Gainesville, FL , United States
– name: 4 Department of Anesthesiology, University of Florida , Gainesville, FL , United States
– name: 6 Department of Neurosurgery, University of California , San Francisco, CA , United States
– name: 3 Department of Neuroscience, College of Medicine, University of Florida , Gainesville, FL , United States
– name: 5 Department of Neurology, University of California , San Francisco, CA , United States
Author_xml – sequence: 1
  givenname: Joshua M.
  surname: Garcia
  fullname: Garcia, Joshua M.
– sequence: 2
  givenname: Stephanie A.
  surname: Stillings
  fullname: Stillings, Stephanie A.
– sequence: 3
  givenname: Jenna L.
  surname: Leclerc
  fullname: Leclerc, Jenna L.
– sequence: 4
  givenname: Harrison
  surname: Phillips
  fullname: Phillips, Harrison
– sequence: 5
  givenname: Nancy J.
  surname: Edwards
  fullname: Edwards, Nancy J.
– sequence: 6
  givenname: Steven A.
  surname: Robicsek
  fullname: Robicsek, Steven A.
– sequence: 7
  givenname: Brian L.
  surname: Hoh
  fullname: Hoh, Brian L.
– sequence: 8
  givenname: Spiros
  surname: Blackburn
  fullname: Blackburn, Spiros
– sequence: 9
  givenname: Sylvain
  surname: Doré
  fullname: Doré, Sylvain
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28659854$$D View this record in MEDLINE/PubMed
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Copyright Copyright © 2017 Garcia, Stillings, Leclerc, Phillips, Edwards, Robicsek, Hoh, Blackburn and Doré. 2017 Garcia, Stillings, Leclerc, Phillips, Edwards, Robicsek, Hoh, Blackburn and Doré
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Keywords intracerebral hemorrhage
endothelium
vasculature
subarachnoid hemorrhage
traumatic brain injury
concussion
stroke
ischemia
Language English
License This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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Specialty section: This article was submitted to Stroke, a section of the journal Frontiers in Neurology
Reviewed by: Arthur Liesz, Ludwig-Maximilians-Universität München, Germany; Emmanuel Pinteaux, University of Manchester, United Kingdom; Maria-Grazia De Simoni, Istituto Di Ricerche Farmacologiche Mario Negri, Italy
These authors have contributed equally to this work.
Edited by: Jean-Claude Baron, Université Paris Descartes, France
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Snippet Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory...
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StartPage 244
SubjectTerms concussion
endothelium
intracerebral hemorrhage
ischemia
Neuroscience
stroke
subarachnoid hemorrhage
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Title Role of Interleukin-10 in Acute Brain Injuries
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