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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...

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Detalles Bibliográficos
Autores principales: Yao, Yong-ming, Zhang, Hui
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
Descripción
Sumario: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.