Tao Yanyan, Li Miaomiao, Liu Cheng
Department of Emergency Medicine, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.
Institute of Critical Care Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China.
IET Syst Biol. 2024 Dec;18(6):218-226. doi: 10.1049/syb2.12109. Epub 2024 Nov 22.
Sepsis is a severe systemic inflammatory syndrome triggered by infection and is a leading cause of morbidity and mortality in intensive care units (ICUs). Immune dysfunction is a hallmark of sepsis. In this study, the authors investigated cell-cell communication among lymphoid-derived leucocytes using single-cell RNA sequencing (scRNA-seq) to gain a deeper understanding of the underlying mechanisms in late-stage sepsis. The authors' findings revealed that both the number and strength of cellular interactions were elevated in septic patients compared to healthy individuals, with several pathways showing significant alterations, particularly in conventional dendritic cells (cDCs) and plasmacytoid dendritic cells (pDCs). Notably, pathways such as CD6-ALCAM were more activated in sepsis, potentially due to T cell suppression. This study offers new insights into the mechanisms of immunosuppression and provides potential avenues for clinical intervention in sepsis.
脓毒症是一种由感染引发的严重全身性炎症综合征,是重症监护病房(ICU)发病和死亡的主要原因。免疫功能障碍是脓毒症的一个标志。在本研究中,作者使用单细胞RNA测序(scRNA-seq)研究了淋巴来源白细胞之间的细胞间通讯,以更深入地了解晚期脓毒症的潜在机制。作者的研究结果显示,与健康个体相比,脓毒症患者的细胞间相互作用数量和强度均有所增加,有几条信号通路表现出显著变化,特别是在传统树突状细胞(cDCs)和浆细胞样树突状细胞(pDCs)中。值得注意的是,诸如CD6-ALCAM等信号通路在脓毒症中更活跃,这可能是由于T细胞抑制所致。本研究为免疫抑制机制提供了新的见解,并为脓毒症的临床干预提供了潜在途径。