严重烧伤感染后细胞因子风暴发生发展机制浅析

严重烧伤感染早期，机体天然免疫细胞杀伤功能持续低下，引起免疫系统持续代偿性分泌大量细胞因子，以提高抗细菌感染能力；细胞因子分泌一旦失控，就会形成细胞因子风暴。严重烧伤感染后期，持续的急性髓系增生引起的骨髓动员能力耗竭、免疫应答水平低下、促修复的抑炎因子分泌增加，将导致机体处于免疫抑制状态。烧伤感染后，细胞因子风暴是由过度的促炎刺激、炎症调节不足或两者共同引起。本文拟从免疫学角度，就严重烧伤感染后机体抗病原菌感染免疫反应的改变进程，严重烧伤感染早期细胞因子风暴和后期机体免疫抑制状态的发生及转化机制做一简要总结。未来研究方向建议从以下方面展开:严重烧伤后先天免疫细胞细菌杀伤功能低下的机制，急性髓系增生导致髓系抑制细胞（MDSC）和有核红细胞增多在细胞因子风暴发生发展过程中的作用机制，巨噬细胞吞噬杀伤细菌功能障碍与分泌细胞因子功能亢进的关键调节机制，巨噬细胞M1型/M2型以及效应T细胞/调节性T细胞动态平衡破坏在引发机体免疫抑制状态中作用及关键调节机制。

Analysis of the Development Mechanism of Cytokine Storm in Severe Burn Patients Complicated with Infection

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.