Whole blood DNA methylation analysis reveals respiratory environmental traits involved in COVID-19 severity following SARS-CoV-2 infection.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
06 08 2022
Historique:
received: 28 07 2021
accepted: 26 07 2022
entrez: 6 8 2022
pubmed: 7 8 2022
medline: 10 8 2022
Statut: epublish

Résumé

SARS-CoV-2 infection can cause an inflammatory syndrome (COVID-19) leading, in many cases, to bilateral pneumonia, severe dyspnea, and in ~5% of these, death. DNA methylation is known to play an important role in the regulation of the immune processes behind COVID-19 progression, however it has not been studied in depth. In this study, we aim to evaluate the implication of DNA methylation in COVID-19 progression by means of a genome-wide DNA methylation analysis combined with DNA genotyping. The results reveal the existence of epigenomic regulation of functional pathways associated with COVID-19 progression and mediated by genetic loci. We find an environmental trait-related signature that discriminates mild from severe cases and regulates, among other cytokines, IL-6 expression via the transcription factor CEBP. The analyses suggest that an interaction between environmental contribution, genetics, and epigenetics might be playing a role in triggering the cytokine storm described in the most severe cases.

Identifiants

pubmed: 35933486
doi: 10.1038/s41467-022-32357-2
pii: 10.1038/s41467-022-32357-2
pmc: PMC9357033
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4597

Informations de copyright

© 2022. The Author(s).

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Auteurs

Guillermo Barturen (G)

GENYO. Center for Genomics and Oncological Research Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain. guillermo.barturen@genyo.es.

Elena Carnero-Montoro (E)

GENYO. Center for Genomics and Oncological Research Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.

Manuel Martínez-Bueno (M)

GENYO. Center for Genomics and Oncological Research Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.

Silvia Rojo-Rello (S)

Servicio de Microbiología e Inmunología, Hospital Clínico Universitario de Valladolid, Valladolid, Spain.

Beatriz Sobrino (B)

Servicio de Enfermedades Infecciosas, Hospital Regional de Málaga, Málaga, Spain.
IBIMA. Instituto de Investigación Biomédica de Málaga, Málaga, Spain.

Óscar Porras-Perales (Ó)

Servicio de Enfermedades Infecciosas, Hospital Regional de Málaga, Málaga, Spain.
IBIMA. Instituto de Investigación Biomédica de Málaga, Málaga, Spain.

Clara Alcántara-Domínguez (C)

Lorgen G.P., S.L., Business Innovation Center - BIC/CEEL, Technological Area of Health Science, Granada, Spain.

David Bernardo (D)

Mucosal Immunology Lab. Unidad de Excelencia Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM, Universidad de Valladolid-CSIC), Valladolid, Spain.
Centro de Investigaciones Biomédicas en Red en Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.

Marta E Alarcón-Riquelme (ME)

GENYO. Center for Genomics and Oncological Research Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain. marta.alarcon@genyo.es.
Unit of Inflammatory Chronic Diseases, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. marta.alarcon@genyo.es.

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