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基于多组学的抗炎免疫特征表征了新冠后综合征。

A multi-omics based anti-inflammatory immune signature characterizes long COVID-19 syndrome.

作者信息

Kovarik Johannes J, Bileck Andrea, Hagn Gerhard, Meier-Menches Samuel M, Frey Tobias, Kaempf Anna, Hollenstein Marlene, Shoumariyeh Tarik, Skos Lukas, Reiter Birgit, Gerner Marlene C, Spannbauer Andreas, Hasimbegovic Ena, Schmidl Doreen, Garhöfer Gerhard, Gyöngyösi Mariann, Schmetterer Klaus G, Gerner Christopher

机构信息

Department of Internal Medicine III, Clinical Division of Nephrology and Dialysis, Medical University of Vienna, Waehringer Gürtel 18-20, Vienna 1090, Austria.

Joint Metabolome Facility, Faculty of Chemistry, University of Vienna, Waehringer Straße 38, 1090 Vienna, Austria.

出版信息

iScience. 2023 Jan 20;26(1):105717. doi: 10.1016/j.isci.2022.105717. Epub 2022 Dec 5.

DOI:10.1016/j.isci.2022.105717
PMID:36507225
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9719844/
Abstract

To investigate long COVID-19 syndrome (LCS) pathophysiology, we performed an exploratory study with blood plasma derived from three groups: 1) healthy vaccinated individuals without SARS-CoV-2 exposure; 2) asymptomatic recovered patients at least three months after SARS-CoV-2 infection and; 3) symptomatic patients at least 3 months after SARS-CoV-2 infection with chronic fatigue syndrome or similar symptoms, here designated as patients with long COVID-19 syndrome (LCS). Multiplex cytokine profiling indicated slightly elevated pro-inflammatory cytokine levels in recovered individuals in contrast to patients with LCS. Plasma proteomics demonstrated low levels of acute phase proteins and macrophage-derived secreted proteins in LCS. High levels of anti-inflammatory oxylipins including omega-3 fatty acids in LCS were detected by eicosadomics, whereas targeted metabolic profiling indicated high levels of anti-inflammatory osmolytes taurine and hypaphorine, but low amino acid and triglyceride levels and deregulated acylcarnitines. A model considering alternatively polarized macrophages as a major contributor to these molecular alterations is presented.

摘要

为了研究新冠长期综合征(LCS)的病理生理学,我们进行了一项探索性研究,使用了来自三组人群的血浆:1)未接触过SARS-CoV-2的健康接种者;2)SARS-CoV-2感染后至少三个月的无症状康复患者;3)SARS-CoV-2感染后至少三个月出现慢性疲劳综合征或类似症状的有症状患者,此处称为新冠长期综合征(LCS)患者。多重细胞因子分析表明,与LCS患者相比,康复个体的促炎细胞因子水平略有升高。血浆蛋白质组学显示LCS患者急性期蛋白和巨噬细胞衍生分泌蛋白水平较低。通过类二十烷酸组学检测到LCS患者中包括ω-3脂肪酸在内的高水平抗炎氧化脂质,而靶向代谢分析表明抗炎渗透剂牛磺酸和hypaphorine水平较高,但氨基酸和甘油三酯水平较低且酰基肉碱失调。本文提出了一个模型,认为交替极化的巨噬细胞是这些分子改变的主要促成因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/1582e378f262/gr5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/79afb81f563b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/35992876669e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/1c279884de05/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/ca76d1970f01/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/1582e378f262/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/8fdd6b46b0f9/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/79afb81f563b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/35992876669e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/1c279884de05/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/ca76d1970f01/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/184e/9771720/1582e378f262/gr5.jpg

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