Department of Medicine, Stony Brook University, Stony Brook, New York, USA.
Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
J Clin Invest. 2020 Nov 2;130(11):5674-5676. doi: 10.1172/JCI142780.
In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.
在极短的时间内，由严重急性呼吸系统综合征冠状病毒 2（SARS-CoV-2）引起的突发冠状病毒病 2019（COVID-19）疫情让毫无准备的世界陷入混乱。尽管病毒的传播速度确实令人措手不及，但世界各地的科学家一直在努力破解 SARS-CoV-2 诱导多系统和多器官炎症反应的机制，这些反应共同导致受影响个体的高死亡率。在本期 JCI 中，Skendros 和 Mitsios 等人就是这样的一个团队，他们报告称，补体系统在引发似乎导致 COVID-19 严重程度的过度炎症和血栓性微血管病方面发挥了重要作用。为了支持补体系统以及中性粒细胞和血小板共同导致 COVID-19 的假说，作者提供了实证证据，表明补体抑制剂 compstatin Cp40 的治疗抑制了中性粒细胞中组织因子的表达。这些结果证实了补体轴的关键作用，并表明使用补体抑制剂的靶向治疗是治疗 COVID-19 诱导炎症的潜在治疗选择。
