Author: Sarma, A.; Christenson, S. A.; Mick, E.; DeVoe, C.; Deiss, T.; Pisco, A. O.; Ghale, R.; Jauregui, A.; Byrne, A.; Moazed, F.; Spottiswoode, N.; Sinha, P.; Zha, B. S.; Serpa, P. H.; Ansel, K. M.; Wilson, J. G.; Leligdowicz, A.; Siegel, E. R.; Sirota, M.; DeRisi, J. L.; Matthay, M. A.; COMET Consortium,; Hendrickson, C. M.; Kangelaris, K. N.; Krummel, M.; Woodruff, P. G.; Erle, D. J.; Calfee, C. S.; Langelier, C. R.
Title: COVID-19 ARDS is characterized by a dysregulated host response that differs from cytokine storm and may be modified by dexamethasone Cord-id: x6akbo5f Document date: 2021_1_4
ID: x6akbo5f
Snippet: 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.
Document: 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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