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血浆磷脂:一种评估新冠病毒感染严重程度的有前景的简单生化参数。

Plasma Phospholipids: A Promising Simple Biochemical Parameter to Evaluate COVID-19 Infection Severity.

作者信息

Hussein Mohammed Abdalla, Ismail Noor Eldin Mohamed, Mohamed Ahmed H, Borik Rita M, Ali Ali Abdelaziz, Mosaad Yasser O

机构信息

Department of Biochemistry, Faculty of Applied Medical Science, October 6 University, 6th of October City, Egypt.

Consultant in hest chronic diseases, Shobra Health Insurance Hospital, Shobra, Egypt.

出版信息

Bioinform Biol Insights. 2021 Nov 18;15:11779322211055891. doi: 10.1177/11779322211055891. eCollection 2021.

DOI:10.1177/11779322211055891
PMID:34840499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8619733/
Abstract

BACKGROUND

Coronavirus-19 (COVID-19) pandemic is a worldwide public health problem that has been known in China since December 25, 2019. Phospholipids are structural components of the mammalian cytoskeleton and cell membranes. They suppress viral attachment to the plasma membrane and subsequent replication in lung cells. In the virus-infected lung, phospholipids are highly prone to oxidation by reactive oxygen species, leading to the production of oxidized phospholipids (OxPLs).

OBJECTIVE

This study was carried out to explain the correlation between the level of plasma phospholipids in patients with COVID-19 infection and the levels of cytokine storms to assess the severity of the disease.

METHODS

Plasma samples from 34 enrolled patients with mild, moderate, and severe COVID-19 infection were collected. Complete blood count (CBC), plasma levels of D-dimer, ferritin, C-reactive protein (CRP), cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), phospholipids, secretory phospholipase A2 (sPLA2)α2, and cytokine storms were estimated, and lung computed tomography (CT) imaging was detected.

RESULTS

The CBC picture showed the presence of leukopenia, lymphopenia, and eosinopenia in patients with COVID-19 infection. Furthermore, a significant increase was found in plasma levels of D-dimer, CRP, ferritin, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-13 as well as sPLA2α2 activity compared to normal persons. However, plasma levels of phospholipids decreased in patients with moderate and severe COVID-19 infection, as well as significantly decreased in levels of triacylglycerols and HDL-C in plasma from patients with severe infection only, compared to normal persons. Furthermore, a lung CT scan showed the presence of inflammation in a patient with mild, moderate, and severe COVID-19 infection.

CONCLUSIONS

This study shows that there is a correlation between plasma phospholipid depletion and elevated cytokine storm in patients with COVID-19 infection. Depletion of plasma phospholipid levels in patients with COVID-19 infection is due to oxidative stress, induction of cytokine storm, and systemic inflammatory response after endothelial cell damage promote coagulation. According to current knowledge, patients with COVID-19 infection may need to administer surfactant replacement therapy and sPLA2 inhibitors to treat respiratory distress syndrome, which helps them to maintain the interconnected surfactant structures.

摘要

背景

新型冠状病毒肺炎(COVID-19)大流行是一个全球性的公共卫生问题,自2019年12月25日起在中国被发现。磷脂是哺乳动物细胞骨架和细胞膜的结构成分。它们可抑制病毒附着于质膜并随后在肺细胞中复制。在病毒感染的肺中,磷脂极易被活性氧氧化,导致氧化磷脂(OxPLs)的产生。

目的

本研究旨在解释COVID-19感染患者血浆磷脂水平与细胞因子风暴水平之间的相关性,以评估疾病的严重程度。

方法

收集34例入选的轻度、中度和重度COVID-19感染患者的血浆样本。检测全血细胞计数(CBC)、血浆D-二聚体、铁蛋白、C反应蛋白(CRP)、胆固醇、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、磷脂、分泌型磷脂酶A2(sPLA2)α2水平以及细胞因子风暴,并进行肺部计算机断层扫描(CT)成像检测。

结果

CBC结果显示COVID-19感染患者存在白细胞减少、淋巴细胞减少和嗜酸性粒细胞减少。此外,与正常人相比,患者血浆D-二聚体、CRP、铁蛋白、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6和IL-13水平以及sPLA2α2活性显著升高。然而,中度和重度COVID-19感染患者的血浆磷脂水平降低,仅重度感染患者的血浆三酰甘油和HDL-C水平与正常人相比显著降低。此外,肺部CT扫描显示轻度、中度和重度COVID-19感染患者均存在炎症。

结论

本研究表明,COVID-19感染患者血浆磷脂消耗与细胞因子风暴升高之间存在相关性。COVID-19感染患者血浆磷脂水平的消耗是由于氧化应激、细胞因子风暴的诱导以及内皮细胞损伤后的全身炎症反应促进凝血所致。根据目前的认识,COVID-19感染患者可能需要进行表面活性剂替代治疗和sPLA2抑制剂治疗呼吸窘迫综合征,这有助于维持相互连接的表面活性剂结构。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/2c5a4a40ef8c/10.1177_11779322211055891-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/5c9a5513b997/10.1177_11779322211055891-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/390cb632f6de/10.1177_11779322211055891-fig2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/a6dfecebded0/10.1177_11779322211055891-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/2c5a4a40ef8c/10.1177_11779322211055891-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/5c9a5513b997/10.1177_11779322211055891-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/390cb632f6de/10.1177_11779322211055891-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/ae995f8a140f/10.1177_11779322211055891-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/a6dfecebded0/10.1177_11779322211055891-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ce/8619733/2c5a4a40ef8c/10.1177_11779322211055891-fig5.jpg

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