Evidence map›Paper›PMID 36443794›Full record

ArticleGenome medicine2022

Epigenetic and transcriptomic reprogramming in monocytes of severe COVID-19 patients reflects alterations in myeloid differentiation and the influence of inflammatory cytokines.

Gerard Godoy-Tena, Anis Barmada, Octavio Morante-Palacios, Carlos de la Calle-Fabregat, Ricardo Martins-Ferreira, Anna G Ferreté-Bonastre, Laura Ciudad, Adolfo Ruiz-Sanmartín, Mónica Martínez-Gallo, Ricard Ferrer and 4 more

Abstract read
In one paragraph

Article in Genome medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. iScience · 2026
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  7. Induction of dysfunctional CD14Frontiers in immunology · 2026
    Article
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  14. Immune Homeostasis: A Novel Example of Teamwork.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
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  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Gerard Godoy-TenaEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Anis BarmadaWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, CB10 1RQ, UK.
Octavio Morante-PalaciosEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Carlos de la Calle-FabregatEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Ricardo Martins-FerreiraEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Anna G Ferreté-BonastreEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Laura CiudadEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Adolfo Ruiz-SanmartínIntensive Care Department, Vall d'Hebron University Hospital, Shock, Organ Dysfunction and Resuscitation (SODIR) Research Group, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, 08035, Barcelona, Spain.
Mónica Martínez-GalloImmunology Division, Vall d'Hebron University Hospital and Diagnostic Immunology Research Group, Vall d'Hebron Research Institute (VHIR), 08035, Barcelona, Spain.
Ricard FerrerIntensive Care Department, Vall d'Hebron University Hospital, Shock, Organ Dysfunction and Resuscitation (SODIR) Research Group, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, 08035, Barcelona, Spain.
Juan Carlos Ruiz-RodriguezIntensive Care Department, Vall d'Hebron University Hospital, Shock, Organ Dysfunction and Resuscitation (SODIR) Research Group, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona, 08035, Barcelona, Spain.
Javier Rodríguez-UbrevaEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain.
Roser Vento-TormoWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, CB10 1RQ, UK.
Esteban BallestarEpigenetics and Immune Disease Group, Josep Carreras Research Institute (IJC), 08916, Badalona, Barcelona, Spain. eballestar@carrerasresearch.org.ORCID 0000-0002-1400-2440

Funding

Wellcome Trust WT206194
6 · The paper itself

Abstract

backgroundCOVID-19 manifests with a wide spectrum of clinical phenotypes, ranging from asymptomatic and mild to severe and critical. Severe and critical COVID-19 patients are characterized by marked changes in the myeloid compartment, especially monocytes. However, little is known about the epigenetic alterations that occur in these cells during hyperinflammatory responses in severe COVID-19 patients.

methodsIn this study, we obtained the DNA methylome and transcriptome of peripheral blood monocytes from severe COVID-19 patients. DNA samples extracted from CD14 + CD15- monocytes of 48 severe COVID-19 patients and 11 healthy controls were hybridized on MethylationEPIC BeadChip arrays. In parallel, single-cell transcriptomics of 10 severe COVID-19 patients were generated. CellPhoneDB was used to infer changes in the crosstalk between monocytes and other immune cell types.

resultsWe observed DNA methylation changes in CpG sites associated with interferon-related genes and genes associated with antigen presentation, concordant with gene expression changes. These changes significantly overlapped with those occurring in bacterial sepsis, although specific DNA methylation alterations in genes specific to viral infection were also identified. We also found these alterations to comprise some of the DNA methylation changes occurring during myeloid differentiation and under the influence of inflammatory cytokines. A progression of DNA methylation alterations in relation to the Sequential Organ Failure Assessment (SOFA) score was found to be related to interferon-related genes and T-helper 1 cell cytokine production. CellPhoneDB analysis of the single-cell transcriptomes of other immune cell types suggested the existence of altered crosstalk between monocytes and other cell types like NK cells and regulatory T cells.

conclusionOur findings show the occurrence of an epigenetic and transcriptional reprogramming of peripheral blood monocytes, which could be associated with the release of aberrant immature monocytes, increased systemic levels of pro-inflammatory cytokines, and changes in immune cell crosstalk in these patients.

Indexed as

COVID-19MonocytesAntiviral AgentsCytokinesEpigenesis, GeneticHumansInterferonsTranscriptomeAntiviral AgentsCytokinesInterferonsCOVID-19DNA methylationEpigenomicsImmune cell crosstalkMonocytesSingle-cell transcriptomics

Identifiers

PMID36443794
PMCPMC9706884

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.