Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts.
Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts.
Am J Pathol. 2021 Jan;191(1):4-17. doi: 10.1016/j.ajpath.2020.08.009. Epub 2020 Sep 11.
The rapid spread of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has resulted in an unprecedented public health crisis worldwide. Recent studies indicate that a hyperinflammatory syndrome induced by SARS-CoV-2 contributes to disease severity and mortality in COVID-19. In this review, an overview of the pathophysiology underlying the hyperinflammatory syndrome in severe COVID-19 is provided. The current evidence suggests that the hyperinflammatory syndrome results from a dysregulated host innate immune response. The gross and microscopic pathologic findings as well as the alterations in the cytokine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophils in severe COVID-19 are summarized. The data highlighted include the potential therapeutic approaches undergoing investigation to modulate the immune response and abrogate lung injury in severe COVID-19.
2019 年冠状病毒病(COVID-19)的迅速传播是由严重急性呼吸系统综合症冠状病毒 2(SARS-CoV-2)引起的,这导致了全球范围内前所未有的公共卫生危机。最近的研究表明,由 SARS-CoV-2 引起的超炎症综合征导致 COVID-19 的严重程度和死亡率增加。在这篇综述中,概述了严重 COVID-19 中超炎症综合征的病理生理学基础。目前的证据表明,超炎症综合征是由宿主先天免疫反应失调引起的。总结了严重 COVID-19 中的大体和显微镜病理发现以及细胞因子环境、巨噬细胞/单核细胞、自然杀伤细胞、T 细胞和中性粒细胞的改变。强调的数据包括正在研究的潜在治疗方法,以调节免疫反应并阻断严重 COVID-19 中的肺损伤。