体外膜肺氧合（ECMO）是各种严重心肺衰竭的有效支持手段，但心脏术后ECMO辅助患者脱ECMO后发生脓毒症死亡是临床面临的重要问题。我们前期研究发现ECMO辅助中患者外周血具有髓源抑制性细胞（MDSCs）表型的髓系细胞增多，但不具备免疫抑制功能，而这些细胞脱离ECMO环路可成为免疫抑制细胞MDSCs。我们推测：ECMO辅助时"接触激活"导致免疫细胞以激活占主导地位，脱机后免疫活化因素降低，髓系细胞可以转化为MDSCs，免疫状态失衡，导致脱机后脓毒症。为验证假说，本课题拟以ECMO支持患者的外周血细胞为研究对象，将脱机后阶段作为关注点，研究髓系细胞的转化和免疫功能的变化，以求明确ECMO脱机后免疫抑制的主要细胞亚群及MDSCs转化或成熟的机制，分析MDSCs与ECMO感染/脓毒症的相关性。为临床预防和干预ECMO脱机后脓毒症提供细胞学基础和理论指导，以期大幅提高ECMO患者存活率。

Extracorporeal membrane oxygenation (ECMO) is effective on a variety of severe cardiac or pulmonary failure patients. However, it is an important problem that some patients, especially who underwent cardiac surgery, suffer sepsis after weaning from ECMO and the sepsis may induce death. Our previous study found that the patients on ECMO support had increased peripheral myeloid cells which own the phenotype of myeloid-derived suppressor cells (MDSCs), but these cells did not have immunosuppressive function. Moreover, after left the environment of ECMO circuit, these cells became immunosuppressive MDSCs. Thus, we speculate that ECMO support causes "contact activation" of immune cells, whereas weaning from ECMO with reduced immune activation factors causes the transformation of myeloid cells to immunosuppressive MDSCs, leads to immunity disequilibrium and sepsis. To verify the hypothesis, this study intends to take the peripheral blood cells from patients undergoing ECMO and post-ECMO supporting. We will observe the dynamic changes and the function changes of myeloid cells in order to clear the main immunosuppressive MDSC subsets, whether the transformation or maturation of MDSCs is mediated by LILRB activation - JAK/STAT3 phosphorylation pathway, and the correlation between MDSCs and ECMO infection / sepsis. We expect to explore the cellular mechanism and provide theoretical guidance for prevention and intervention of post-ECMO sepsis, significantly improve the survival of ECMO-supported patients.