COVID-19 ARDS is characterized by a dysregulated host response that differs from cytokine storm and may be modified by dexamethasone

  1. Aartik Sarma
  2. Stephanie A. Christenson
  3. Eran Mick
  4. Catherine DeVoe
  5. Thomas Deiss
  6. Angela Oliveira Pisco
  7. Rajani Ghale
  8. Alejandra Jauregui
  9. Ashley Byrne
  10. Farzad Moazed
  11. Natasha Spottiswoode
  12. Pratik Sinha
  13. Beth Shoshana Zha
  14. Paula Hayakawa Serpa
  15. K. Mark Ansel
  16. Jennifer G. Wilson
  17. Aleksandra Leligdowicz
  18. Emily R. Siegel
  19. Marina Sirota
  20. Joseph L. DeRisi
  21. Michael A. Matthay
  22. COMET Consortium
  23. Carolyn M. Hendrickson
  24. Kirsten N. Kangelaris
  25. Matthew F. Krummel
  26. Prescott G. Woodruff
  27. David J. Erle
  28. Carolyn S. Calfee
  29. Charles R. Langelier
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Abstract

We performed comparative lower respiratory tract transcriptional profiling of 52 critically ill patients with ARDS from COVID-19 or other etiologies, or without ARDS. We found no evidence of cytokine storm but instead observed complex host response dysregulation driven by genes with non-canonical roles in inflammation and immunity that were predicted to be modulated by dexamethasone. Compared to other viral ARDS, COVID-19 was characterized by impaired interferon-stimulated gene expression.

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