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Research progress of neuroinflammation-related cells in traumatic brain injury: A review
Neuroinflammation after traumatic brain injury (TBI) is related to chronic neurodegenerative diseases and is one of the causes of acute secondary injury after TBI. Therefore, it is particularly important to clarify the role of cellular mechanisms in the neuroinflammatory response after TBI. The obje...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10289497/ https://www.ncbi.nlm.nih.gov/pubmed/37352020 http://dx.doi.org/10.1097/MD.0000000000034009 |
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author | Zhao, Qinghui Li, Huige Li, Hongru Xie, Fei Zhang, Jianhua |
author_facet | Zhao, Qinghui Li, Huige Li, Hongru Xie, Fei Zhang, Jianhua |
author_sort | Zhao, Qinghui |
collection | PubMed |
description | Neuroinflammation after traumatic brain injury (TBI) is related to chronic neurodegenerative diseases and is one of the causes of acute secondary injury after TBI. Therefore, it is particularly important to clarify the role of cellular mechanisms in the neuroinflammatory response after TBI. The objective of this article is to understand the involvement of cells during the TBI inflammatory response (for instance, astrocytes, microglia, and oligodendrocytes) and shed light on the recent progress in the stimulation and interaction of granulocytes and lymphocytes, to provide a novel approach for clinical research. We searched articles in PubMed published between 1950 and 2023, using the following keywords: TBI, neuroinflammation, inflammatory cells, neuroprotection, clinical. Articles for inclusion in this paper were finalized based on their novelty, representativeness, and relevance to the main arguments of this review. We found that the neuroinflammatory response after TBI includes the activation of glial cells, the release of inflammatory mediators in the brain, and the recruitment of peripheral immune cells. These inflammatory responses not only induce secondary brain damage, but also have a role in repairing the nervous system to some extent. However, not all of the mechanisms of cell-to-cell interactions have been well studied. After TBI, clinical treatment cannot simply suppress the inflammatory response, and the inflammatory phenotype of patients’ needs to be defined according to their specific conditions after injury. Clinical trials of personalized inflammation regulation therapy for specific patients should be carried out in order to improve the prognosis of patients. |
format | Online Article Text |
id | pubmed-10289497 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-102894972023-06-24 Research progress of neuroinflammation-related cells in traumatic brain injury: A review Zhao, Qinghui Li, Huige Li, Hongru Xie, Fei Zhang, Jianhua Medicine (Baltimore) 5300 Neuroinflammation after traumatic brain injury (TBI) is related to chronic neurodegenerative diseases and is one of the causes of acute secondary injury after TBI. Therefore, it is particularly important to clarify the role of cellular mechanisms in the neuroinflammatory response after TBI. The objective of this article is to understand the involvement of cells during the TBI inflammatory response (for instance, astrocytes, microglia, and oligodendrocytes) and shed light on the recent progress in the stimulation and interaction of granulocytes and lymphocytes, to provide a novel approach for clinical research. We searched articles in PubMed published between 1950 and 2023, using the following keywords: TBI, neuroinflammation, inflammatory cells, neuroprotection, clinical. Articles for inclusion in this paper were finalized based on their novelty, representativeness, and relevance to the main arguments of this review. We found that the neuroinflammatory response after TBI includes the activation of glial cells, the release of inflammatory mediators in the brain, and the recruitment of peripheral immune cells. These inflammatory responses not only induce secondary brain damage, but also have a role in repairing the nervous system to some extent. However, not all of the mechanisms of cell-to-cell interactions have been well studied. After TBI, clinical treatment cannot simply suppress the inflammatory response, and the inflammatory phenotype of patients’ needs to be defined according to their specific conditions after injury. Clinical trials of personalized inflammation regulation therapy for specific patients should be carried out in order to improve the prognosis of patients. Lippincott Williams & Wilkins 2023-06-23 /pmc/articles/PMC10289497/ /pubmed/37352020 http://dx.doi.org/10.1097/MD.0000000000034009 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY) (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | 5300 Zhao, Qinghui Li, Huige Li, Hongru Xie, Fei Zhang, Jianhua Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title | Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title_full | Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title_fullStr | Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title_full_unstemmed | Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title_short | Research progress of neuroinflammation-related cells in traumatic brain injury: A review |
title_sort | research progress of neuroinflammation-related cells in traumatic brain injury: a review |
topic | 5300 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10289497/ https://www.ncbi.nlm.nih.gov/pubmed/37352020 http://dx.doi.org/10.1097/MD.0000000000034009 |
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