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Acute drivers of neuroinflammation in traumatic brain injury
Neuroinflammation is initiated as a result of traumatic brain injury and can exacerbate evolving tissue pathology. Immune cells respond to acute signals from damaged cells, initiate neuroinflammation, and drive the pathological consequences over time. Importantly, the mechanism(s) of injury, the loc...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6557091/ https://www.ncbi.nlm.nih.gov/pubmed/31089036 http://dx.doi.org/10.4103/1673-5374.255958 |
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author | Wofford, Kathryn L. Loane, David J. Cullen, D. Kacy |
author_facet | Wofford, Kathryn L. Loane, David J. Cullen, D. Kacy |
author_sort | Wofford, Kathryn L. |
collection | PubMed |
description | Neuroinflammation is initiated as a result of traumatic brain injury and can exacerbate evolving tissue pathology. Immune cells respond to acute signals from damaged cells, initiate neuroinflammation, and drive the pathological consequences over time. Importantly, the mechanism(s) of injury, the location of the immune cells within the brain, and the animal species all contribute to immune cell behavior following traumatic brain injury. Understanding the signals that initiate neuroinflammation and the context in which they appear may be critical for understanding immune cell contributions to pathology and regeneration. Within this paper, we review a number of factors that could affect immune cell behavior acutely following traumatic brain injury. |
format | Online Article Text |
id | pubmed-6557091 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-65570912019-09-01 Acute drivers of neuroinflammation in traumatic brain injury Wofford, Kathryn L. Loane, David J. Cullen, D. Kacy Neural Regen Res Review Neuroinflammation is initiated as a result of traumatic brain injury and can exacerbate evolving tissue pathology. Immune cells respond to acute signals from damaged cells, initiate neuroinflammation, and drive the pathological consequences over time. Importantly, the mechanism(s) of injury, the location of the immune cells within the brain, and the animal species all contribute to immune cell behavior following traumatic brain injury. Understanding the signals that initiate neuroinflammation and the context in which they appear may be critical for understanding immune cell contributions to pathology and regeneration. Within this paper, we review a number of factors that could affect immune cell behavior acutely following traumatic brain injury. Wolters Kluwer - Medknow 2019-09 /pmc/articles/PMC6557091/ /pubmed/31089036 http://dx.doi.org/10.4103/1673-5374.255958 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/4.0 This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Review Wofford, Kathryn L. Loane, David J. Cullen, D. Kacy Acute drivers of neuroinflammation in traumatic brain injury |
title | Acute drivers of neuroinflammation in traumatic brain injury |
title_full | Acute drivers of neuroinflammation in traumatic brain injury |
title_fullStr | Acute drivers of neuroinflammation in traumatic brain injury |
title_full_unstemmed | Acute drivers of neuroinflammation in traumatic brain injury |
title_short | Acute drivers of neuroinflammation in traumatic brain injury |
title_sort | acute drivers of neuroinflammation in traumatic brain injury |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6557091/ https://www.ncbi.nlm.nih.gov/pubmed/31089036 http://dx.doi.org/10.4103/1673-5374.255958 |
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