脓毒症（Sepsis）是指由感染引起的宿主反应失调的全身炎症反应综合征（SIRS），继而导致危及生命的器官功能失调，其中严重脓毒症死亡率接近50%，临床治疗方案的革新和优化极为急迫。脓毒症表现为先天免疫细胞的数量增加与后天免疫细胞的数量减少，其中PD-L1+的中性粒细胞的数量增加更为明显，而针对其的治疗研究尚属空白。我们之前建立了盲肠结扎穿孔术（CLP）的大鼠脓毒症模型，发现瓜氨酸预处理可以有效对抗脓毒症造成的肠等多器官功能损伤。在此模型中，我们准备检测PD-L1+的中性粒细胞的变化差异，分析瓜氨酸预处理、阿特珠单抗（PD-L1抗体）阻断及两者联合使用对PD-L1+的中性粒细胞的变化趋势的影响，并检测它们的肠损伤差异。通过对相关样本的RNA-seq测序，进行分子机制初探。最终，为免疫治疗在脓毒症临床防治选择上提供实验和理论基础。

Sepsis is a systemic inflammatory response syndrome (SIRS) caused by infection, which in turn leads to life-threatening organ dysfunction. The mortality rate of severe sepsis is close to 50%, therefore, the innovation and optimization of clinical treatment are very urgent. Sepsis is characterized by an increase in the number of innate immune cells and a decrease in the number of acquired immune cells, in which the number of PD-L1+ neutrophils increases more significantly, however, the therapeutic study on it is still blank. We have previously established a rat sepsis model with cecal ligation and puncture (CLP), and found that citrulline pretreatment could effectively combat sepsis and organs dysfunction, such as intestinal damage. In this study, The changes of PD-L1+ neutrophils will be detected. The effects of citrulline pretreatment, atezolizumab(PD-L1 antibody) blocking and their combination on the PD-L1+ neutrophil trend and intestinal injury will be analyzed. Through the RNA-seq sequencing of related samples, the molecular mechanism will be explored premilinarily. Finally, it provides an experimental and theoretical basis for immunotherapy in the clinical prevention and treatment of sepsis.