Janicova Andrea, Relja Borna
Experimental Radiology, University Clinic for Radiology and Nuclear Medicine, Otto von Guericke University Magdeburg, Magdeburg, Germany.
Shock. 2021 Jul 1;56(1):16-29. doi: 10.1097/SHK.0000000000001695.
Physical trauma is one of the leading causes of mortality worldwide. Early post-traumatic upregulation of the pro-inflammatory immune response to traumatic injury is paralleled by an anti-inflammatory reaction. A prevalence of each has been associated with the development of secondary complications, including nosocomial infections, acute lung injury, acute respiratory distress syndrome, sepsis, and death after trauma. There is accumulating evidence that neutrophils, which are known to provide the first line of defense against invading pathogens or harmful agents, are considerably involved in the initiation and propagation of the inflammatory response to traumatic injury. In this review, we summarize and discuss recent findings about the impact of trauma and trauma-related sepsis as a secondary complication on neutrophil biology, which constitutes as the interface between homeostasis and tissue damage after a traumatic insult. Here, patient cohorts of physically injured patients with an overall injury severity score above 9 have been considered, including patients with blunt as well as penetrating injuries, and sepsis. Mechanisms were replenished by animal studies. Altered antigen presentation on neutrophils has been shown to possess biomarker features predicting both outcome and vulnerability to infectious complications in severely injured patients. Dysregulated activation of neutrophils following trauma affects their functions including phagocytizing capacity, production of reactive oxygen species, formation of neutrophil extracellular traps, which all together have been associated with the development of secondary complications. Thus, we highlight neutrophils and their functions as potential future targets for optimizing post-traumatic treatment strategies, which potentially may improve patient outcomes.
身体创伤是全球主要的死亡原因之一。创伤后早期对创伤性损伤的促炎免疫反应上调的同时会出现抗炎反应。每种反应的普遍存在都与继发性并发症的发生有关,包括医院感染、急性肺损伤、急性呼吸窘迫综合征、败血症以及创伤后死亡。越来越多的证据表明,已知作为抵御入侵病原体或有害物质第一道防线的中性粒细胞,在创伤性损伤炎症反应的启动和传播中起重要作用。在这篇综述中,我们总结并讨论了关于创伤及作为继发性并发症的创伤相关败血症对中性粒细胞生物学影响的最新研究结果,中性粒细胞生物学构成了创伤性损伤后体内平衡与组织损伤之间的界面。这里,我们考虑了总体损伤严重程度评分高于9分的身体受伤患者队列,包括钝性伤和穿透伤患者以及败血症患者。通过动物研究补充了相关机制。已表明中性粒细胞上抗原呈递的改变具有预测重伤患者结局和感染并发症易感性的生物标志物特征。创伤后中性粒细胞的失调激活会影响其功能,包括吞噬能力、活性氧的产生、中性粒细胞胞外陷阱的形成,所有这些都与继发性并发症的发生有关。因此,我们强调中性粒细胞及其功能是优化创伤后治疗策略的潜在未来靶点,这可能会改善患者预后。