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COVID-19 ARDS is characterized by a dysregulated host response that differs from cytokine storm and is modified by dexamethasone.
Sarma, Aartik; Christenson, Stephanie A; Mick, Eran; DeVoe, Catherine; Deiss, Thomas; Pisco, Angela Oliveira; Ghale, Rajani; Jauregui, Alejandra; Byrne, Ashley; Moazed, Farzad; Spottiswoode, Natasha; Sinha, Pratik; Zha, Beth Shoshana; Neff, Norma; Tan, Michelle; Serpa, Paula Hayakawa; Ansel, K Mark; Wilson, Jennifer G; Leligdowicz, Aleksandra; Siegel, Emily R; Sirota, Marina; DeRisi, Joseph L; Matthay, Michael A; Hendrickson, Carolyn M; Kangelaris, Kirsten N; Krummel, Matthew F; Woodruff, Prescott G; Erle, David J; Calfee, Carolyn S; Langelier, Charles R.
Afiliação
  • Sarma A; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Christenson SA; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Mick E; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • DeVoe C; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Deiss T; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Pisco AO; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Ghale R; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Jauregui A; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Byrne A; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Moazed F; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Spottiswoode N; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Sinha P; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Zha BS; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Neff N; Department of Medicine, University of California, San Francisco, CA, USA.
  • Tan M; Department of Anesthesia, Washington University, Saint Louis, Missouri, MO, USA.
  • Serpa PH; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Ansel KM; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Wilson JG; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Leligdowicz A; Division of Infectious Diseases, University of California, San Francisco, CA, USA.
  • Siegel ER; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Sirota M; Department of Microbiology and Immunology, University of California, San Francisco, CA, USA.
  • DeRisi JL; Sandler Asthma Basic Research Center, University of California, San Francisco, CA, USA.
  • Matthay MA; Department of Emergency Medicine, Stanford University, Palo Alto, CA, USA.
  • Hendrickson CM; School of Medicine, University of California, San Francisco, CA, USA.
  • Kangelaris KN; Division of Rheumatology, University of California, San Francisco, CA, USA.
  • Krummel MF; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Woodruff PG; Department of Biochemistry and Biophysics, University of California, San Francisco, CA, USA.
  • Erle DJ; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
  • Langelier CR; Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, CA, USA.
Res Sq ; 2021 Jan 14.
Article em En | MEDLINE | ID: mdl-33469573
ABSTRACT
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Revista: Res Sq Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Revista: Res Sq Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos