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Inflammatory Response Following Diffuse Axonal Injury

DAI is a leading cause of the patient's death or lasting vegetable state following severe TBI, and up to now the detailed mechanism of axonal injury after head trauma is still unclear. Inflammatory responses have been proved to be an important mechanism of neural injury after TBI. However, most...

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Detalles Bibliográficos
Autores principales: Lin, Yu, Wen, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607236/
https://www.ncbi.nlm.nih.gov/pubmed/23532682
http://dx.doi.org/10.7150/ijms.5423
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author Lin, Yu
Wen, Liang
author_facet Lin, Yu
Wen, Liang
author_sort Lin, Yu
collection PubMed
description DAI is a leading cause of the patient's death or lasting vegetable state following severe TBI, and up to now the detailed mechanism of axonal injury after head trauma is still unclear. Inflammatory responses have been proved to be an important mechanism of neural injury after TBI. However, most of these studies are concerned with focal cerebral injury following head trauma. In contrast to focal injury, studies on the inflammatory reaction following DAI are only beginning. And in this article, we aimed to review such studies. From the studies reviewed, immune response cells would become reactive around the sites of axonal injury after DAI. Besides, the concentrations of several important inflammatory factors, such as IL-1 family, IL-6 and TNF-ɑ, increased after DAI as well, which implies the participation of inflammatory responses. It can be concluded that inflammatory responses probably participate in the neural injury in DAI, but at present the study of inflammatory responses following DAI is still limited and the clear effects of inflammatory response on axonal injury remain to be more explored.
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spelling pubmed-36072362013-03-25 Inflammatory Response Following Diffuse Axonal Injury Lin, Yu Wen, Liang Int J Med Sci Review DAI is a leading cause of the patient's death or lasting vegetable state following severe TBI, and up to now the detailed mechanism of axonal injury after head trauma is still unclear. Inflammatory responses have been proved to be an important mechanism of neural injury after TBI. However, most of these studies are concerned with focal cerebral injury following head trauma. In contrast to focal injury, studies on the inflammatory reaction following DAI are only beginning. And in this article, we aimed to review such studies. From the studies reviewed, immune response cells would become reactive around the sites of axonal injury after DAI. Besides, the concentrations of several important inflammatory factors, such as IL-1 family, IL-6 and TNF-ɑ, increased after DAI as well, which implies the participation of inflammatory responses. It can be concluded that inflammatory responses probably participate in the neural injury in DAI, but at present the study of inflammatory responses following DAI is still limited and the clear effects of inflammatory response on axonal injury remain to be more explored. Ivyspring International Publisher 2013-03-13 /pmc/articles/PMC3607236/ /pubmed/23532682 http://dx.doi.org/10.7150/ijms.5423 Text en © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
spellingShingle Review
Lin, Yu
Wen, Liang
Inflammatory Response Following Diffuse Axonal Injury
title Inflammatory Response Following Diffuse Axonal Injury
title_full Inflammatory Response Following Diffuse Axonal Injury
title_fullStr Inflammatory Response Following Diffuse Axonal Injury
title_full_unstemmed Inflammatory Response Following Diffuse Axonal Injury
title_short Inflammatory Response Following Diffuse Axonal Injury
title_sort inflammatory response following diffuse axonal injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607236/
https://www.ncbi.nlm.nih.gov/pubmed/23532682
http://dx.doi.org/10.7150/ijms.5423
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