COVID-19 ARDS is characterized by a dysregulated host response that differs from cytokine storm and is modified by dexamethasone.
Journal
Research square
Titre abrégé: Res Sq
Pays: United States
ID NLM: 101768035
Informations de publication
Date de publication:
14 Jan 2021
14 Jan 2021
Historique:
entrez:
20
1
2021
pubmed:
21
1
2021
medline:
21
1
2021
Statut:
epublish
Résumé
We performed comparative lower respiratory tract transcriptional profiling of 52 critically ill patients with the acute respiratory distress syndrome (ARDS) from COVID-19 or from other etiologies, as well as controls without ARDS. In contrast to a cytokine storm, we observed reduced proinflammatory gene expression in COVID-19 ARDS when compared to ARDS due to other causes. COVID-19 ARDS was characterized by a dysregulated host response with increased PTEN signaling and elevated expression of genes with non-canonical roles in inflammation and immunity that were predicted to be modulated by dexamethasone and granulocyte colony stimulating factor. Compared to ARDS due to other types of viral pneumonia, COVID-19 was characterized by impaired interferon-stimulated gene expression (ISG). We found that the relationship between SARS-CoV-2 viral load and expression of ISGs was decoupled in patients with COVID-19 ARDS when compared to patients with mild COVID-19. In summary, assessment of host gene expression in the lower airways of patients with COVID-19 ARDS did not demonstrate cytokine storm but instead revealed a unique and dysregulated host response predicted to be modified by dexamethasone.
Identifiants
pubmed: 33469573
doi: 10.21203/rs.3.rs-141578/v1
pmc: PMC7814832
pii:
doi:
Types de publication
Preprint
Langues
eng
Subventions
Organisme : NHLBI NIH HHS
ID : K23 HL138461
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI007641
Pays : United States
Commentaires et corrections
Type : UpdateIn
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