Sepsis has a systemic inflammatory response syndrome caused by infection. While neutrophils play contradictory roles in different stages of sepsis. Neutrophils have been proven to play an antibacterial role by producing neutrophil extracellular traps (NETs). Although the NET is beneficial to bacteria resistance, abnormal NET increases tissue damage. The complement C5a receptor 1 (C5ar1) is a gene related to strong inflammatory reactions and is found to be associated with inflammatory factors. This study found that there were 45 down-regulated genes and 704 up-regulated genes in sepsis rats by transcriptome sequencing. And those genes were significantly related to inflammation and immunity by GO and KEGG enrichment analysis involving the chemokine signaling pathway, the Toll-like receptor (TLR) signaling pathway, and the Fc gamma R-mediated phagocytosis. Additionally, the C5ar1 gene was significantly upregulated with interesting potential in sepsis and used for further study. This study used cecum ligation and puncture (CLP) rats that were respectively injected intravenously with PBS or the lentivirus vector to explore the effect of C5ar1 on CLP rats. It demonstrated that silenced- C5ar1 inhibited the ALT, AST, BUN, and CREA levels, improved the lung and spleen injury, and reduced the TNF-α, IL-6, IL-1β, IL-10, cf-DNA, and cfDNA/MPO levels. Additionally, silenced C5ar1 inhibited the TLR2, TLR4, and peptidylarginine deiminase 4 expression levels, which suggested the improvement of silenced C5ar1 on sepsis via inhibiting NETs and the TLR signaling pathway. This study provides a basis and new direction for the study of treatment on sepsis.

脓毒症是由感染引起的全身炎症反应综合征。而中性粒细胞在脓毒症的不同阶段发挥着矛盾的作用。中性粒细胞已被证明通过产生中性粒细胞胞外陷阱（NET）来发挥抗菌作用。虽然NET有利于细菌抵抗，但异常的NET会增加组织损伤。补体C5a受体1（C5ar1）是与强烈炎症反应相关的基因，被发现与炎症因子有关。本研究通过转录组测序发现脓毒症大鼠中有45个下调基因和704个上调基因。通过GO和KEGG富集分析，这些基因与炎症和免疫显着相关，涉及趋化因子信号通路、Toll样受体（TLR）信号通路和FcγR介导的吞噬作用。此外，C5ar1 基因显着上调，在败血症中具有令人感兴趣的潜力，可用于进一步研究。本研究采用盲肠结扎穿刺（CLP）大鼠，分别静脉注射PBS或慢病毒载体，探讨C5ar1对CLP大鼠的影响。结果表明，沉默的C5ar1可抑制ALT、AST、BUN和CREA水平，改善肺和脾损伤，并降低TNF-α、IL-6、IL-1β、IL-10、cf-DNA和cfDNA /MPO 水平。此外，沉默的 C5ar1 抑制 TLR2、TLR4 和肽基精氨酸脱亚胺酶 4 的表达水平，这表明沉默的 C5ar1 通过抑制 NET 和 TLR 信号通路改善脓毒症。该研究为脓毒症治疗研究提供了基础和新方向。