PDF(Pubmed)
Abstract：
BACKGROUND: Understanding the enduring respiratory consequences of severe COVID-19 is crucial for comprehensive patient care. This study aims to evaluate the impact of post-COVID conditions on respiratory sequelae of severe acute respiratory distress syndrome (ARDS).
METHODS: We examined 88 survivors of COVID-19-associated severe ARDS six months post-intensive care unit (ICU) discharge. Assessments included clinical and functional evaluation as well as plasma biomarkers of endothelial dysfunction, inflammation, and viral response. Additionally, an in vitro model using human umbilical vein endothelial cells (HUVECs) explored the direct impact of post-COVID plasma on endothelial function.
RESULTS: Post-COVID patients with impaired gas exchange demonstrated persistent endothelial inflammation marked by elevated ICAM-1, IL-8, CCL-2, and ET-1 plasma levels. Concurrently, systemic inflammation, evidenced by NLRP3 overexpression and elevated levels of IL-6, sCD40-L, and C-reactive protein, was associated with endothelial dysfunction biomarkers and increased in post-COVID patients with impaired gas exchange. T-cell activation, reflected in CD69 expression, and persistently elevated levels of interferon-β (IFN-β) further contributed to sustained inflammation. The in vitro model confirmed that patient plasma, with altered levels of sCD40-L and IFN-β proteins, has the capacity to alter endothelial function.
CONCLUSIONS: Six months post-ICU discharge, survivors of COVID-19-associated ARDS exhibited sustained elevation in endothelial dysfunction biomarkers, correlating with the severity of impaired gas exchange. NLRP3 inflammasome activity and persistent T-cell activation indicate on going inflammation contributing to persistent endothelial dysfunction, potentially intensified by sustained viral immune response.
METHODS: We examined 88 survivors of COVID-19-associated severe ARDS six months post-intensive care unit (ICU) discharge. Assessments included clinical and functional evaluation as well as plasma biomarkers of endothelial dysfunction, inflammation, and viral response. Additionally, an in vitro model using human umbilical vein endothelial cells (HUVECs) explored the direct impact of post-COVID plasma on endothelial function.
RESULTS: Post-COVID patients with impaired gas exchange demonstrated persistent endothelial inflammation marked by elevated ICAM-1, IL-8, CCL-2, and ET-1 plasma levels. Concurrently, systemic inflammation, evidenced by NLRP3 overexpression and elevated levels of IL-6, sCD40-L, and C-reactive protein, was associated with endothelial dysfunction biomarkers and increased in post-COVID patients with impaired gas exchange. T-cell activation, reflected in CD69 expression, and persistently elevated levels of interferon-β (IFN-β) further contributed to sustained inflammation. The in vitro model confirmed that patient plasma, with altered levels of sCD40-L and IFN-β proteins, has the capacity to alter endothelial function.
CONCLUSIONS: Six months post-ICU discharge, survivors of COVID-19-associated ARDS exhibited sustained elevation in endothelial dysfunction biomarkers, correlating with the severity of impaired gas exchange. NLRP3 inflammasome activity and persistent T-cell activation indicate on going inflammation contributing to persistent endothelial dysfunction, potentially intensified by sustained viral immune response.
摘要：
背景：了解严重COVID-19的持久呼吸后果对于全面的患者护理至关重要。本研究旨在评估COVID后条件对严重急性呼吸窘迫综合征（ARDS）的呼吸后遗症的影响。
方法：我们检查了重症监护病房（ICU）出院后6个月的88名COVID-19相关严重ARDS幸存者。评估包括临床和功能评估以及内皮功能障碍的血浆生物标志物，炎症,和病毒反应。此外,使用人脐静脉内皮细胞(HUVECs)的体外模型研究了COVID后血浆对内皮功能的直接影响.
结果：COVID后气体交换受损患者表现出持续的内皮炎症，表现为ICAM-1，IL-8，CCL-2和ET-1血浆水平升高。同时,全身性炎症,NLRP3过表达和IL-6，sCD40-L，和C反应蛋白,与内皮功能障碍生物标志物相关，并且在患有气体交换受损的COVID后患者中增加。T细胞激活,反映在CD69表达中，持续升高的干扰素-β（IFN-β）水平进一步导致持续的炎症。体外模型证实，患者血浆，随着sCD40-L和IFN-β蛋白水平的改变，有能力改变内皮功能.
结论：ICU出院后六个月，COVID-19相关ARDS的幸存者表现出内皮功能障碍生物标志物的持续升高，与气体交换受损的严重程度相关。NLRP3炎性体活性和持续的T细胞活化表明持续的炎症有助于持续的内皮功能障碍，持续的病毒免疫反应可能会加剧。
方法：我们检查了重症监护病房（ICU）出院后6个月的88名COVID-19相关严重ARDS幸存者。评估包括临床和功能评估以及内皮功能障碍的血浆生物标志物，炎症,和病毒反应。此外,使用人脐静脉内皮细胞(HUVECs)的体外模型研究了COVID后血浆对内皮功能的直接影响.
结果：COVID后气体交换受损患者表现出持续的内皮炎症，表现为ICAM-1，IL-8，CCL-2和ET-1血浆水平升高。同时,全身性炎症,NLRP3过表达和IL-6，sCD40-L，和C反应蛋白,与内皮功能障碍生物标志物相关，并且在患有气体交换受损的COVID后患者中增加。T细胞激活,反映在CD69表达中，持续升高的干扰素-β（IFN-β）水平进一步导致持续的炎症。体外模型证实，患者血浆，随着sCD40-L和IFN-β蛋白水平的改变，有能力改变内皮功能.
结论：ICU出院后六个月，COVID-19相关ARDS的幸存者表现出内皮功能障碍生物标志物的持续升高，与气体交换受损的严重程度相关。NLRP3炎性体活性和持续的T细胞活化表明持续的炎症有助于持续的内皮功能障碍，持续的病毒免疫反应可能会加剧。
