链球菌引发宿主中毒性休克综合症相关机制的研究进展

某些链球菌在感染过程中,会引发宿主系统性的细胞因子风暴,病程进展迅速,致死率高,即发生链球菌性中毒性休克综合症(streptococcal toxic shock syndrome,STSS)。最初认为STSS由链球菌的超抗原(superantigen,SAg)引发,但近年来也有不依赖超抗原的STSS病例报道,致病机制较为复杂。本文主要对不依赖链球菌超抗原引发STSS的机制研究进行介绍,包括链球菌感染后宿主细胞中炎症信号通路的激活、炎性小体和细胞焦亡的发生、促炎细胞因子的释放以及细胞因子风暴等。同时,对研究链球菌STSS常采用的细胞和动物模型进行总结,旨在为实验室开展STSS的机制研究奠定理论基础。

Host toxic shock syndrome induced by Streptococcus

Streptococcal toxic shock syndrome (STSS) is a rapidly progressing, life-threatening, systemic reaction to invasive infection caused by streptococci, which is characterized by a cytokine storm in the host. Although the majority of clinical STSS cases are triggered by the superantigens (SAgs), a few STSS cases are not associated with SAgs and the related mechanisms are considered to be complicated. Here, we review the recent research progress on the mechanism of SAgs-independent STSS, including the activation of inflammatory signaling pathways in host triggered by Streptococcus,the activation of inflammatosomes and pyroptosis, the pro-inflammatory cytokines and cytokine storm. We also summarize cell and animal models usually used in STSS research. This review is useful for a better understanding of STSS and provides a theoretical foundation for the research of STSS mechanism.