Trauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Fucheng Road 51, Haidian District, Beijing, 100048, People's Republic of China.
Mil Med Res. 2019 Jul 25;6(1):23. doi: 10.1186/s40779-019-0214-9.
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.
在现代战争中,战斗损伤的治疗是提高人员生存率和战斗力的关键问题。由于受到遥远战场恶劣环境的限制,无法提供快速有效的治疗,导致感染、败血症、多器官功能障碍综合征(MODS)和高死亡率。为了获得更好的战斗损伤治疗效果,我们总结了最近在《MMR》上发表的几项与败血症和 MODS 机制相关的报告。Chaudry 及其同事报告了创伤、休克和败血症的性别差异。女性的有利结果归因于她们的激素环境。他们的累积报告表明,雌激素是包括中枢神经系统、心肺系统、肝脏、肾脏、免疫系统等多个系统和器官的有益因素,可提高败血症的生存率。Thompson 等人综述了创伤引起的败血症的潜在机制,可归结为损伤相关分子模式(DAMPs)和其他免疫调节因子触发的免疫反应失衡。他们还强调免疫调节作为一种更好的治疗策略的潜力,可能在调节宿主免疫反应方面具有潜在益处。Fan 等人揭示了肺上皮细胞和巨噬细胞相互作用的关键机制,其中涉及白细胞介素 25(IL-25)作为介质。损伤后,肺上皮细胞分泌的 IL-25 促进巨噬细胞中 TNF-α的产生,导致急性肺损伤(ALI)。除了大量细胞因子外,免疫细胞中线粒体功能障碍也是败血症期间免疫功能障碍的另一个关键危险因素。线粒体的形态和功能改变与 ATP 产生不足、代谢过程不足和 ROS 产生超负荷密切相关,通过触发氧化应激,导致免疫细胞和其他组织受损。上述所有报告都讨论了创伤后败血症的诱导机制,并提供了针对不同危险因素的更好治疗策略的证据。