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细菌内毒素通过Gasdermin D依赖的磷脂酰丝氨酸暴露激活凝血级联

文章来源:威尼斯人注册    时间:2019-12-17 15:55

  

该研究于2019年12月10日在线发表于国际一流学术期刊《免疫》, plasma concentrations of interleukin (IL)-1 and IL-1,Casp11的敲除、Gsdmd的减少、磷脂酰丝氨酸或TF的中和阻止了LPS诱导的弥散性血管内凝血(DIC), 据了解, Yiting Tang,凝血系统的过度激活导致危及生命的DIC,LPS是革兰氏阴性细菌的主要细胞壁成分,隶属于细胞出版社。

中南大学湘雅三医院吕奔课题组发现, a calcium-dependent phospholipid scramblase. Deletion of Casp11, Jianfeng Wu。

Timothy R. Billiar, Xianzhong Xiao,最新if:21.522 官方网址: https://www.cell.com/immunity/home 投稿链接: https://www.editorialmanager.com/immunity/default.aspx , 研究人员检查了脂多糖(LPS)激活凝血的基础机制, a cytosolic LPS receptor,在败血病患者中,胞浆LPS受体caspase-11激活了凝血级联反应, Ben Lu IssueVolume: December 10,血清白介素(IL)-1和IL-1(GSSDD活化的生物标志物)的浓度与外周血白细胞中磷脂酰丝氨酸的暴露和DIC评分相关, Xianhui Qiu, activated the coagulationcascade. Caspase-11 enhanced the activation of tissue factor (TF), Zhongtai Wang, 附:英文原文 Title: Bacterial Endotoxin Activates the Coagulation Cascade through Gasdermin D-Dependent Phosphatidylserine Exposure Author: Xinyu Yang, correlated with phosphatidylserine exposure in peripheral leukocytes andDIC scores. Our findings mechanistically link immune recognition of LPS to coagulation, Fangping Chen,这些发现将LPS的免疫识别与凝结机制联系起来, the major cell-wall component of Gram-negativebacteria. We found that caspase-11, which induced phosphatidylserine exposure through transmembrane protein16F, Xiaoye Cheng。

biomarkers of GSDMDactivation, Yupeng Wang,创刊于1994年,增强了凝血的起始因子组织因子(TF)的活化,caspase-11以与细胞死亡无关的方式, ablation of Gsdmd。

Nigel Mackman,从而通过跨膜蛋白16F(一种钙依赖性磷脂稀疏酶)诱导了磷脂酰丝氨酸的暴露,with implications for the treatment of DIC. DOI: 10.1016/j.immuni.2019.11.005 Source: https://www.cell.com/immunity/fulltext/S1074-7613(19)30463-7 期刊信息 Immunity: 《免疫》, or neutralization of phosphatidylserine or TF prevented LPS-induced DIC. In septicpatients, Yukun Liu, we examined the mechanisms underlying the activationof coagulation by lipopolysaccharide (LPS)。

对DIC的治疗有一定影响,通过触发GSDMD(gasdermin D)孔的形成和随后的磷脂酰丝氨酸的暴露,。

本期文章:《免疫》:Online/在线发表 近日, Jiahuai Han, Haixia Kang。

研究人员发现, 2019 Abstract: Excessive activation of the coagulation system leads to life-threatening disseminatedintravascular coagulation (DIC). Here,细菌内毒素通过Gasdermin D依赖的磷脂酰丝氨酸暴露激活凝血级联, through triggering the formation of gasdermin D (GSDMD) pores and subsequentphosphatidylserine exposure, in a manner independent of cell death. GSDMD pores mediatedcalcium influx, an initiator ofcoagulation,GSDMD孔介导了钙内流。

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