A multi-omics based anti-inflammatory immune signature characterizes long COVID-19 syndrome.
Immunology
immune response
omics
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
20 Jan 2023
20 Jan 2023
Historique:
received:
17
08
2022
revised:
13
10
2022
accepted:
29
11
2022
pubmed:
13
12
2022
medline:
13
12
2022
entrez:
12
12
2022
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 36507225
doi: 10.1016/j.isci.2022.105717
pii: S2589-0042(22)01990-3
pmc: PMC9719844
doi:
Types de publication
Journal Article
Langues
eng
Pagination
105717Informations de copyright
© 2022 The Author(s).
Déclaration de conflit d'intérêts
The authors CG, KS, SMM, JK, AB and MG have filed a patent application to the European Patent Office with the application number EP22176741 (date June 1st. 2022) and the title:” METHODS AND MEANS FOR MOLECULAR CHARACTERIZATION OF POST-VIRAL FATIGUE SYNDROME.” The other authors declare no competing interests.
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