Selenium (Se) deficiency and poor plasma Se levels can cause cardiovascular diseases by decreasing selenoprotein levels. Neutrophil extracellular traps (NETs) may be the vicious cycle center of inflammation in vasculitis. Here, we show that Se deficiency induced arteritis mainly by reducing selenoprotein S (SelS), and promoted the progression of arteritis by regulating the recruitment of neutrophils and NET formation. Silencing SelS induced chicken arterial endothelial cells (PAECs) to secrete cytokines, and activated neutrophils to promote NET formation. Conversely, scavenging DNA-NETs promoted cytokine secretion in PAECs. The NET formation regulated by siSelS was dependent on a reactive oxygen species (ROS) burst. We also found that the PPAR pathway was a major mediator of NET formation induced by Se-deficient arteritis. Overall, our results reveal how Se deficiency regulates NET formation in the progression of arteritis and support silencing-SelS worsens arteritis.

硒缺乏和血浆硒水平低会通过降低硒蛋白水平而引起心血管疾病。中性粒细胞外陷阱（NETs）可能是血管炎中炎症的恶性循环中心。在这里，我们表明，硒缺乏症主要通过减少硒蛋白S（SelS）来诱导动脉炎，并通过调节中性粒细胞的募集和NET的形成促进了动脉炎的发展。沉默SelS诱导鸡动脉内皮细胞（PAEC）分泌细胞因子，并激活嗜中性粒细胞以促进NET的形成。相反，清除DNA-NETs可促进PAEC中细胞因子的分泌。siSelS调节的NET形成取决于活性氧（ROS）爆发。我们还发现，PPAR途径是由Se缺乏性动脉炎诱导的NET形成的主要介体。全面的，