Activated neutrophils release neutrophil extracellular traps (NETs) in response to a variety of stimuli. NETosis is driven by protein-arginine deiminase type 4, with the release of intracellular granule components that function by capturing and destroying microbes, including viral, fungal, bacterial, and protozoal pathogens. The positive effects of pathogen control are countered by pro-inflammatory effects as demonstrated in a variety of diseases. Components of NETS are non-specific, and other than controlling microbes, they cause injury to surrounding tissue by themselves or by increasing the pro-inflammatory response. NETs can play a role in enhancement of the inflammation seen in autoimmune diseases including psoriasis, rheumatoid arthritis, and systemic lupus erythematosis. In addition, autoinflammatory diseases such as gout have been associated with NETosis. Inhibition of NETs may decrease the severity of many diseases improving survival. Herein, we describe NETosis in different diseases focusing on the detrimental effect of NETs and outline possible therapeutics that can be used to mitigate netosis. There is a need for more studies and clinical trials on these and other compounds that could prevent or destroy NETs, thereby decreasing damage to patients.

激活的中性粒细胞响应各种刺激而释放中性粒细胞胞外陷阱（NET）。 NETosis 由 4 型蛋白质精氨酸脱亚胺酶驱动，释放细胞内颗粒成分，通过捕获和破坏微生物（包括病毒、真菌、细菌和原生动物病原体）发挥作用。正如多种疾病所证明的那样，病原体控制的积极作用会被促炎作用所抵消。 NETS 的成分是非特异性的，除了控制微生物之外，它们本身或通过增加促炎反应对周围组织造成损伤。 NETs 可以增强自身免疫性疾病的炎症，包括牛皮癣、类风湿性关节炎和系统性红斑狼疮。此外，痛风等自身炎症性疾病也与 NETosis 相关。抑制 NET 可能会降低许多疾病的严重程度，从而提高生存率。在此，我们描述了不同疾病中的 NETosis，重点关注 NET 的有害影响，并概述了可用于减轻 netosis 的可能治疗方法。需要对这些和其他可以预防或破坏 NET 的化合物进行更多的研究和临床试验，从而减少对患者的伤害。