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解析 COVID-19 和 STEMI 中失控免疫反应的线索:知识共享的新需求。

Unraveling the thread of uncontrolled immune response in COVID-19 and STEMI: an emerging need for knowledge sharing.

机构信息

INCLIVA Health Research Institute, University of Valencia, Valencia, Spain.

Department of Medicine, School of Medicine, University of Valencia, Valencia, Spain.

出版信息

Am J Physiol Heart Circ Physiol. 2021 Jun 1;320(6):H2240-H2254. doi: 10.1152/ajpheart.00934.2020. Epub 2021 Apr 12.

Abstract

The outbreak of severe acute respiratory syndrome coronavirus 2 that first emerged in Wuhan in December 2019 has resulted in the devastating pandemic of coronavirus disease 2019, creating an emerging need for knowledge sharing. Meanwhile, myocardial infarction is and will probably remain the foremost cause of death in the Western world throughout the coming decades. Severe deregulation of the immune system can unnecessarily expand the inflammatory response and participate in target and multiple organ failure, in infection but also in critical illness. Indeed, the course and fate of inflammatory cells observed in severe ST-elevation myocardial infarction (neutrophilia, monocytosis, and lymphopenia) almost perfectly mirror those recently reported in severe coronavirus disease 2019. A pleiotropic proinflammatory imbalance hampers adaptive immunity in favor of uncontrolled innate immunity and is associated with poorer structural and clinical outcomes. The goal of the present review is to gain greater insight into the cellular and molecular mechanisms underlying this canonical activation and downregulation of the two arms of the immune response in both entities, to better understand their pathophysiology and to open the door to innovative therapeutic options. Knowledge sharing can pave the way for therapies with the potential to significantly reduce mortality in both infectious and noninfectious scenarios.

摘要

2019 年 12 月在中国武汉首次出现的严重急性呼吸综合征冠状病毒 2 的爆发导致了 2019 年冠状病毒病的毁灭性大流行,这就产生了知识共享的新需求。同时,心肌梗死在未来几十年仍将是西方世界首要的死亡原因。免疫系统的严重失调会不必要地扩大炎症反应,并参与靶器官和多器官衰竭,不仅在感染中,而且在危重病中也是如此。事实上,在严重 ST 段抬高型心肌梗死中观察到的炎症细胞的过程和命运(中性粒细胞增多症、单核细胞增多症和淋巴细胞减少症)几乎与最近在严重 2019 年冠状病毒病中报告的完全一致。多种促炎失衡阻碍了适应性免疫,有利于不受控制的固有免疫,并与较差的结构和临床结局相关。本综述的目的是更深入地了解这两种实体中免疫反应的两个分支的细胞和分子机制的基础,以更好地了解其病理生理学,并为创新的治疗选择打开大门。知识共享可以为治疗方法铺平道路,有潜力显著降低感染和非感染性情况下的死亡率。

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