Potentiation of NETs release is novel characteristic of TREM-1 activation and the pharmacological inhibition of TREM-1 could prevent from the deleterious consequences of NETs release in sepsis  

作　　者：Amir Boufenzer Kevin Carrasco Lucie Jolly Benjamin Brustolin Elisa Di-Pillo Marc Derive Sébastien Gibot 

机构地区：[1]INOTREM,Vandœuvre-lès-Nancy,Nancy,France [2]UMR-S 1116,Défaillance Cardiovasculaire Aigue et Chronique,Vandœuvre-lès-Nancy,Nancy,France [3]CHRU Nancy,Hôpital Central,Service de Réanimation Médicale,Nancy,France

出　　处：《Cellular & Molecular Immunology》2021年第2期452-460,共9页中国免疫学杂志（英文版）

摘　　要：During sepsis,neutrophil activation induces endothelial cell(EC)dysfunction partly through neutrophil extracellular trap(NET)release.The triggering receptor expressed on myeloid cell-1(TREM-1)is an orphan immune receptor that amplifies the inflammatory response mediated by Toll-like receptor-4(TLR4)engagement.Although the key role of TLR4 signaling in NETosis is known,the role of TREM-1 in this process has not yet been investigated.Here,we report that TREM-1 potentiates NET release by human and murine neutrophils and is a component of the NET structure.In contrast,pharmacologic inhibition or genetic ablation of TREM-1 decreased NETosis in vitro and during experimental septic shock in vivo.Moreover,isolated NETs were able to activate ECs and impair vascular reactivity,and these deleterious effects were dampened by TREM-1 inhibition.TREM-1 may,therefore,constitute a new therapeutic target to prevent NETosis and associated endothelial dysfunction.

关 键 词：TREM-1 NETS SEPSIS endothelial cell activation vascular dysfunction LR12 

分 类 号：R515.3[医药卫生—内科学]