Center for Inflammation Research, VIB, Ghent, Belgium.
Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
EMBO Rep. 2023 Aug 3;24(8):e57615. doi: 10.15252/embr.202357615. Epub 2023 Jun 26.
Sepsis is the result of a dysregulated host response to an infection and causes high morbidity and mortality at the intensive care units worldwide. Despite intensive research, the current management of sepsis is supportive rather than curative. Therefore, new therapeutic interventions for sepsis and septic shock patients are urgently needed. In this issue of EMBO Reports, Fang et al have used rat sepsis models to show that macrophage-expressed SPNS2, a major transporter of S1P, is a crucial mediator of metabolic reprogramming of macrophages during sepsis which regulates inflammation via the lactate-ROS axis.
败血症是宿主对感染的失调反应的结果，在全球重症监护病房导致高发病率和死亡率。尽管进行了深入研究，但败血症的当前治疗仍是支持性的，而不是治愈性的。因此，迫切需要为败血症和感染性休克患者提供新的治疗干预措施。在本期的《EMBO 报告》中，Fang 等人利用大鼠败血症模型表明，巨噬细胞表达的 SPNS2 是 S1P 的主要转运体，是败血症期间巨噬细胞代谢重编程的关键介质，通过乳酸盐-ROS 轴调节炎症。
