NO₂ has been known to impair immunity and exacerbate susceptibility to infectious diseases. However, scant notice has been taken of the effect of NO₂ on neutrophils. Neutrophil extracellular traps (NETs) formation is necessary for NETosis development by neutrophils as an immune system against pathogens. By analyzing the morphology and signature components of NETs, we focused for the first time on finding that 10 ppm of NO₂ exposure for 15 consecutive days can hinder the formation of NETs. Next, we used NO₂ in vivo derivatives to probe the mechanism for NETs formation in vitro. Our findings showed that NO₂ suppression of respiratory burst levels and mitogen-activated protein kinase (MAPK)/Phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT) signaling was related to NO₂ reduction in NETs formation. Inhibition of phorbol myristate acetate (PMA)-induced NETs formation by NO₂ hindered autophagy, as evidenced by increased mTOR protein expression, decreased LC3 protein expression, and reduced autophagic vesicles. By activating mTOR-mediated autophagy, rapamycin (Rapa) reduced the inhibition of PMA-induced NETs by NO₂. This study will provide valuable insights into the mechanisms of immunotoxicity of NO₂, new insights into the etiology of diseases linked to NETs formation, and a theoretical basis for protection against such illnesses.

众所周知，NO _{2会损害免疫力并加剧对传染病的易感性。}然而，人们很少注意到NO ₂对中性粒细胞的影响。中性粒细胞胞外陷阱 (NET) 的形成对于中性粒细胞作为对抗病原体的免疫系统发展 NETosis 是必要的。通过分析 NET 的形态和特征成分，我们首次发现连续 15 天暴露于 10 ppm 的 NO ₂会阻碍 NET 的形成。接下来，我们使用NO ₂体内衍生物来探讨体外NETs形成的机制。我们的研究结果表明，NO ₂呼吸爆发水平和丝裂原激活蛋白激酶 (MAPK)/磷酸肌醇 3-激酶 (PI3K)-蛋白激酶 B (AKT) 信号传导的抑制与NET 形成中NO ₂的减少有关。_{NO 2}抑制佛波醇肉豆蔻酸酯乙酸酯 (PMA) 诱导的 NET 形成会阻碍自噬，这一点可以通过 mTOR 蛋白表达增加、LC3 蛋白表达减少和自噬囊泡减少来证明。_{通过激活 mTOR 介导的自噬，雷帕霉素 (Rapa) 减少了 NO 2}对 PMA 诱导的 NET 的抑制。_{这项研究将为NO 2}的免疫毒性机制提供有价值的见解，为与NETs形成相关的疾病的病因学提供新的见解，并为预防此类疾病提供理论基础。