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Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI

Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast w...

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Autores principales: Gama Sosa, Miguel A., De Gasperi, Rita, Perez Garcia, Georgina S., Sosa, Heidi, Searcy, Courtney, Vargas, Danielle, Janssen, Pierce L., Perez, Gissel M., Tschiffely, Anna E., Janssen, William G., McCarron, Richard M., Hof, Patrick R., Haghighi, Fatemeh G., Ahlers, Stephen T., Elder, Gregory A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6389215/
https://www.ncbi.nlm.nih.gov/pubmed/29126430
http://dx.doi.org/10.1186/s40478-017-0483-z
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author Gama Sosa, Miguel A.
De Gasperi, Rita
Perez Garcia, Georgina S.
Sosa, Heidi
Searcy, Courtney
Vargas, Danielle
Janssen, Pierce L.
Perez, Gissel M.
Tschiffely, Anna E.
Janssen, William G.
McCarron, Richard M.
Hof, Patrick R.
Haghighi, Fatemeh G.
Ahlers, Stephen T.
Elder, Gregory A.
author_facet Gama Sosa, Miguel A.
De Gasperi, Rita
Perez Garcia, Georgina S.
Sosa, Heidi
Searcy, Courtney
Vargas, Danielle
Janssen, Pierce L.
Perez, Gissel M.
Tschiffely, Anna E.
Janssen, William G.
McCarron, Richard M.
Hof, Patrick R.
Haghighi, Fatemeh G.
Ahlers, Stephen T.
Elder, Gregory A.
author_sort Gama Sosa, Miguel A.
collection PubMed
description Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast waves disrupt the blood-brain barrier, triggering microglial activation and neuroinflammation. Recently, there has been much interest in the role that ongoing neuroinflammation may play in the chronic effects of TBI. Here, we investigated whether chronic neuroinflammation is present in a rat model of repetitive low-energy blast exposure. Six weeks after three 74.5-kPa blast exposures, and in the absence of hemorrhage, no significant alteration in the level of microglia activation was found. At 6 weeks after blast exposure, plasma levels of fractalkine, interleukin-1β, lipopolysaccharide-inducible CXC chemokine, macrophage inflammatory protein 1α, and vascular endothelial growth factor were decreased. However, no differences in cytokine levels were detected between blast-exposed and control rats at 40 weeks. In brain, isolated changes were seen in levels of selected cytokines at 6 weeks following blast exposure, but none of these changes was found in both hemispheres or at 40 weeks after blast exposure. Notably, one animal with a focal hemorrhagic tear showed chronic microglial activation around the lesion 16 weeks post-blast exposure. These findings suggest that focal hemorrhage can trigger chronic focal neuroinflammation following blast-induced TBI, but that in the absence of hemorrhage, chronic neuroinflammation is not a general feature of low-level blast injury.
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spelling pubmed-63892152019-03-19 Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI Gama Sosa, Miguel A. De Gasperi, Rita Perez Garcia, Georgina S. Sosa, Heidi Searcy, Courtney Vargas, Danielle Janssen, Pierce L. Perez, Gissel M. Tschiffely, Anna E. Janssen, William G. McCarron, Richard M. Hof, Patrick R. Haghighi, Fatemeh G. Ahlers, Stephen T. Elder, Gregory A. Acta Neuropathol Commun Research Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast waves disrupt the blood-brain barrier, triggering microglial activation and neuroinflammation. Recently, there has been much interest in the role that ongoing neuroinflammation may play in the chronic effects of TBI. Here, we investigated whether chronic neuroinflammation is present in a rat model of repetitive low-energy blast exposure. Six weeks after three 74.5-kPa blast exposures, and in the absence of hemorrhage, no significant alteration in the level of microglia activation was found. At 6 weeks after blast exposure, plasma levels of fractalkine, interleukin-1β, lipopolysaccharide-inducible CXC chemokine, macrophage inflammatory protein 1α, and vascular endothelial growth factor were decreased. However, no differences in cytokine levels were detected between blast-exposed and control rats at 40 weeks. In brain, isolated changes were seen in levels of selected cytokines at 6 weeks following blast exposure, but none of these changes was found in both hemispheres or at 40 weeks after blast exposure. Notably, one animal with a focal hemorrhagic tear showed chronic microglial activation around the lesion 16 weeks post-blast exposure. These findings suggest that focal hemorrhage can trigger chronic focal neuroinflammation following blast-induced TBI, but that in the absence of hemorrhage, chronic neuroinflammation is not a general feature of low-level blast injury. BioMed Central 2017-11-10 /pmc/articles/PMC6389215/ /pubmed/29126430 http://dx.doi.org/10.1186/s40478-017-0483-z Text en © US Government (outside the USA) 2017 The article is a work of the United States Government; Title 17 U.S.C 105 provides that copyright protection is not available for any work of the United States government in the United States. Additionally, this is an open access article distributed under the terms of the Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0), which permits worldwide unrestricted use, distribution, and reproduction in any medium for any lawful purpose.
spellingShingle Research
Gama Sosa, Miguel A.
De Gasperi, Rita
Perez Garcia, Georgina S.
Sosa, Heidi
Searcy, Courtney
Vargas, Danielle
Janssen, Pierce L.
Perez, Gissel M.
Tschiffely, Anna E.
Janssen, William G.
McCarron, Richard M.
Hof, Patrick R.
Haghighi, Fatemeh G.
Ahlers, Stephen T.
Elder, Gregory A.
Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title_full Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title_fullStr Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title_full_unstemmed Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title_short Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
title_sort lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced tbi
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6389215/
https://www.ncbi.nlm.nih.gov/pubmed/29126430
http://dx.doi.org/10.1186/s40478-017-0483-z
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