Tang Yuan-Yang, Lou Gao-Xing, He Wei-Feng
State Key Laboratory of Trauma, Burns, and Combined Injury, Institute of Burn Research, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing Key Laboratory for Disease Proteomics, Chongqing 400038, China.
Bioengineering College of Chongqing University, Chongqing 400044, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2021 Jan;52(1):16-21. doi: 10.12182/20210160206.
In the early stage of infection in severe burn patients, the killing function of the natural immune cells is continuously low, which causes the immune system to continuously and compensatorily secrete a large amount of cytokines to improve the ability to resist bacterial infection. Once the cytokine secretion is out of control, a cytokine storm will form. In the late stage of severe burn infection, the bone marrow mobilization caused by continuous acute myelodysplasia will be exhausted, the level of immune response will be low, and the secretion of anti-inflammatory factors promoting repair will be increased, which will lead to immune suppression. Cytokine storm after burn infection is caused by excessive proinflammatory stimulation, inadequate inflammatory regulation, or a combination of the two. From the perspective of immunology, this review will briefly summarize the changing process of immune response against pathogenic bacteria after severe burn infection, cytokine storm in the early stage of severe burn infection and the mechanism of occurrence and transformation of immunosuppression in the late stage of severe burn infection. We suggest that future research direction from the following aspects: Mechanism of low bacterial killing function of innate immune cells after severe burns; The mechanism by which acute myeloid hyperplasia leads to myeloid inhibitory cells (MDSC) and nucleated erythrocytosis during the development of cytokine storms; The key regulatory mechanism between macrophage phagocytic dysfunction and cytokine hyperactivity; The role and key regulatory mechanism of destruction of the dynamic balance of M1/M2 macrophages and effector/regulatory T cells in triggering immune suppression.
在严重烧伤患者感染的早期,天然免疫细胞的杀伤功能持续低下,这导致免疫系统持续代偿性分泌大量细胞因子以提高抵抗细菌感染的能力。一旦细胞因子分泌失控,就会形成细胞因子风暴。在严重烧伤感染的后期,持续的急性骨髓发育异常导致的骨髓动员将耗竭,免疫反应水平降低,促进修复的抗炎因子分泌增加,从而导致免疫抑制。烧伤感染后的细胞因子风暴是由促炎刺激过度、炎症调节不足或两者共同作用引起的。从免疫学角度,本综述将简要总结严重烧伤感染后针对病原菌的免疫反应变化过程、严重烧伤感染早期的细胞因子风暴以及严重烧伤感染后期免疫抑制的发生和转变机制。我们建议未来的研究方向如下:严重烧伤后天然免疫细胞细菌杀伤功能低下的机制;急性骨髓增生在细胞因子风暴发生过程中导致髓系抑制细胞(MDSC)和有核红细胞增多的机制;巨噬细胞吞噬功能障碍与细胞因子活性过高之间的关键调节机制;M1/M2巨噬细胞和效应/调节性T细胞动态平衡破坏在触发免疫抑制中的作用及关键调节机制。