Platelet-derived sCD40L: specific inflammatory marker for early-stage severe acute respiratory syndrome coronavirus 2 infection.
Platelet-derived sCD40L: specific inflammatory marker for early-stage severe acute respiratory syndrome coronavirus 2 infection.
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血小板源性sCD40 L:早期严重急性呼吸综合征冠状病毒2感染的特异性炎症标志物
DOI:
10.1186/s12985-021-01680-3
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发表时间:
2021-10-29
期刊:
影响因子:
4.8
通讯作者:
Cognasse F
中科院分区:
文献类型:
--
作者:
Hamzeh-Cognasse H;Mansour A;Reizine F;Mismetti P;Gouin-Thibault I;Cognasse F
The SARS-CoV-2 virus is the causing agent of the Coronavirus disease 2019 (COVID-19) characterized by a huge pro-inflammatory response and coagulation disorders that may lead to for its severe forms, in organ failure or even death. As major players of thrombo-inflammation, platelets release large amounts of immunomodulatory molecules and regulate leukocyte and endothelial activity, which are both altered in COVID-19. Altogether, this makes platelets a very likely actor of the thrombo-inflammatory complications of COVID-19. Thus, we propose to identify a platelet inflammatory signature of severe COVID-19 specifically modulated throughout the course of the disease. Luminex technology and enzyme-linked immunosorbent assay were used to assess plasma levels of platelet inflammatory markers in patients with severe acute respiratory syndrome coronavirus 2 infection on admission and for 14 days afterwards. In accordance with the observations of other teams, we evidence that the plasma levels of the platelet soluble (s)CD40L is significantly elevated in the early stages of the disease. Interestingly we observe that the plasma level of sCD40L decreases overtime while that of sCD62P increases significantly. Our data suggest that there is a platelet signature of inflammatory response to SARS-COv-2 infection which varies overtime and could serve as monitoring biomarkers of patient inflammatory state. Clinical trial registration number: 2020-A01100-39; title: Human Ab Response & immunoMONItoring of COVID-19 Patients, registration date: 05/25/2020; URL of the registry: https://clinicaltrials.gov/ct2/history/NCT04373200?V_5=View.
影响因子:
20.1
作者:
Zaid Y;Puhm F;Allaeys I;Naya A;Oudghiri M;Khalki L;Limami Y;Zaid N;Sadki K;Ben El Haj R;Mahir W;Belayachi L;Belefquih B;Benouda A;Cheikh A;Langlois MA;Cherrah Y;Flamand L;Guessous F;Boilard E
通讯作者:
Boilard E
影响因子:
9.8
作者:
Comer SP;Cullivan S;Szklanna PB;Weiss L;Cullen S;Kelliher S;Smolenski A;Murphy C;Altaie H;Curran J;O'Reilly K;Cotter AG;Marsh B;Gaine S;Mallon P;McCullagh B;Moran N;Ní Áinle F;Kevane B;Maguire PB;COCOON Study investigators
通讯作者:
COCOON Study investigators
DOI:
10.1161/atvbaha.120.314645
发表时间:
2021-01
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
作者:
Portier I;Campbell RA
通讯作者:
Campbell RA