S100A8 may govern hyper-inflammation in severe COVID-19.
S100A8 may govern hyper-inflammation in severe COVID-19.
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DOI：
10.1096/fj.202101013
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发表时间：
2021-09
期刊：
影响因子：
--
通讯作者：
Maru Y
中科院分区：
文献类型：
--
作者：
Deguchi A;Yamamoto T;Shibata N;Maru Y
冠状病毒病2019年(新冠肺炎)大流行威胁人类物种，死亡率约为2%。无论疫苗成功与否，我们都很难预测新冠肺炎的群体免疫时间和结束时间。克服这种情况的一种方法是定义什么是疾病严重程度并作为分子靶标。在慢性髓系白血病的bcr-abl中发现了最成功的类比，它是黄金生物标记物，同时也是最有效的分子靶点。我们推测S100钙结合蛋白A8(S100A8)就是这样一个分子。潜在证据包括：越来越多的临床信息表明S100A8在严重类型的新冠肺炎中表达上调；新冠肺炎与S100A8诱导的急性呼吸窘迫综合征模型之间病变肺的病理相似之处；S100A8是内毒素感受器Toll样受体4/髓系分化蛋白2的内源性配体并在消除了内毒素产生的外源性病原体后仍介导炎症反应的动态平衡理论；新冠肺炎相关急性呼吸窘迫综合征与转移前肺的相似表现，如S100A8上调、肺髓系细胞募集、血管通透性增加和凝血级联反应。用一种能够消除S100A8/S100A9与TLR4相互作用的试剂成功地治疗了动物新冠肺炎模型。在本文中，我们试图验证我们的假设，即S100A8调控新冠肺炎相关的ARDS。
The coronavirus disease 2019 (COVID‐19) pandemic threatens human species with mortality rate of roughly 2%. We can hardly predict the time of herd immunity against and end of COVID‐19 with or without success of vaccine. One way to overcome the situation is to define what delineates disease severity and serves as a molecular target. The most successful analogy is found in BCR‐ABL in chronic myeloid leukemia, which is the golden biomarker, and simultaneously, the most effective molecular target. We hypothesize that S100 calcium‐binding protein A8 (S100A8) is one such molecule. The underlying evidence includes accumulating clinical information that S100A8 is upregulated in severe forms of COVID‐19, pathological similarities of the affected lungs between COVID‐19 and S100A8‐induced acute respiratory distress syndrome (ARDS) model, homeostatic inflammation theory in which S100A8 is an endogenous ligand for endotoxin sensor Toll‐like receptor 4/Myeloid differentiation protein‐2 (TLR4/MD‐2) and mediates hyper‐inflammation even after elimination of endotoxin‐producing extrinsic pathogens, analogous findings between COVID‐19‐associated ARDS and pre‐metastatic lungs such as S100A8 upregulation, pulmonary recruitment of myeloid cells, increased vascular permeability, and activation coagulation cascade. A successful treatment in an animal COVID‐19 model is given with a reagent capable of abrogating interaction between S100A8/S100A9 and TLR4. In this paper, we try to verify our hypothesis that S100A8 governs COVID‐19‐associated ARDS.
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DOI：
10.1016/s1473-3099(20)30773-8
发表时间：
2021-03
期刊：
The Lancet. Infectious diseases
影响因子：
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