Cargando…
Better therapy for combat injury
In modern warfare, therapy for combat injury is a critical issue to improve personnel survival and battle effectiveness. Be limited to the severe circumstance in the distant battlefield, quick and effective treatment cannot be supplied that leads infections, sepsis, multiple organ dysfunction syndro...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6657202/ https://www.ncbi.nlm.nih.gov/pubmed/31340864 http://dx.doi.org/10.1186/s40779-019-0214-9 |
_version_ | 1783438767571337216 |
---|---|
author | Yao, Yong-ming Zhang, Hui |
author_facet | Yao, Yong-ming Zhang, Hui |
author_sort | Yao, Yong-ming |
collection | PubMed |
description | In modern warfare, therapy for combat injury is a critical issue to improve personnel survival and battle effectiveness. Be limited to the severe circumstance in the distant battlefield, quick and effective treatment cannot be supplied that leads infections, sepsis, multiple organ dysfunction syndrome (MODS) and high mortality. To get a better therapy for combat injury, we summarized several reports that associated with the mechanisms of sepsis and MODS, those published on MMR recently. Chaudry and colleagues reported gender difference in the outcomes of trauma, shock and sepsis. The advantageous outcome in female is due to their hormone milieu. Their accumulating reports indicated estrogen as a beneficial factor for multiple system and organs, including the central nervous system, the cardiopulmonary system, the liver, the kidneys, the immune system, and leads to better survival from sepsis. Thompson et al. reviewed the underlying mechanisms in trauma induced sepsis, which can be concluded as an imbalance of immune response triggered by damage-associated molecular patterns (DAMPs) and other immune modifying agents. They also emphasize immunomodulation as a better therapeutic strategy that might be a potential benefit in regulating the host immune response. Fan et al. have revealed a crucial mechanism underlying lung epithelial and macrophage crosstalk, which involves IL-25 as a mediator. After the injury, lung epithelial secreted IL-25 promotes TNF-α production in macrophage leading to acute lung injury (ALI). In addition to a mountain of cytokines, mitochondrial dysfunction in immune cell is another critical risk factor for immune dysfunction during sepsis. Both morphology and function alterations in mitochondria are closely associated with inadequate ATP production, insufficient metabolism process and overloaded ROS production, which lead harm to immune cells and other tissues by triggering oxidative stress. All the above reports discussed mechanisms of sepsis induction after trauma and provided evidence to improve better therapy strategies targeting diverse risk factors. |
format | Online Article Text |
id | pubmed-6657202 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-66572022019-07-31 Better therapy for combat injury Yao, Yong-ming Zhang, Hui Mil Med Res Editorial In modern warfare, therapy for combat injury is a critical issue to improve personnel survival and battle effectiveness. Be limited to the severe circumstance in the distant battlefield, quick and effective treatment cannot be supplied that leads infections, sepsis, multiple organ dysfunction syndrome (MODS) and high mortality. To get a better therapy for combat injury, we summarized several reports that associated with the mechanisms of sepsis and MODS, those published on MMR recently. Chaudry and colleagues reported gender difference in the outcomes of trauma, shock and sepsis. The advantageous outcome in female is due to their hormone milieu. Their accumulating reports indicated estrogen as a beneficial factor for multiple system and organs, including the central nervous system, the cardiopulmonary system, the liver, the kidneys, the immune system, and leads to better survival from sepsis. Thompson et al. reviewed the underlying mechanisms in trauma induced sepsis, which can be concluded as an imbalance of immune response triggered by damage-associated molecular patterns (DAMPs) and other immune modifying agents. They also emphasize immunomodulation as a better therapeutic strategy that might be a potential benefit in regulating the host immune response. Fan et al. have revealed a crucial mechanism underlying lung epithelial and macrophage crosstalk, which involves IL-25 as a mediator. After the injury, lung epithelial secreted IL-25 promotes TNF-α production in macrophage leading to acute lung injury (ALI). In addition to a mountain of cytokines, mitochondrial dysfunction in immune cell is another critical risk factor for immune dysfunction during sepsis. Both morphology and function alterations in mitochondria are closely associated with inadequate ATP production, insufficient metabolism process and overloaded ROS production, which lead harm to immune cells and other tissues by triggering oxidative stress. All the above reports discussed mechanisms of sepsis induction after trauma and provided evidence to improve better therapy strategies targeting diverse risk factors. BioMed Central 2019-07-25 /pmc/articles/PMC6657202/ /pubmed/31340864 http://dx.doi.org/10.1186/s40779-019-0214-9 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Editorial Yao, Yong-ming Zhang, Hui Better therapy for combat injury |
title | Better therapy for combat injury |
title_full | Better therapy for combat injury |
title_fullStr | Better therapy for combat injury |
title_full_unstemmed | Better therapy for combat injury |
title_short | Better therapy for combat injury |
title_sort | better therapy for combat injury |
topic | Editorial |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6657202/ https://www.ncbi.nlm.nih.gov/pubmed/31340864 http://dx.doi.org/10.1186/s40779-019-0214-9 |
work_keys_str_mv | AT yaoyongming bettertherapyforcombatinjury AT zhanghui bettertherapyforcombatinjury |