Author: Satria P. Sajuthi; Peter DeFord; Nathan D. Jackson; Michael T. Montgomery; Jamie L. Everman; Cydney L. Rios; Elmar Pruesse; James D. Nolin; Elizabeth G. Plender; Michael E. Wechsler; Angel CY Mak; Celeste Eng; Sandra Salazar; Vivian Medina; Eric M. Wohlford; Scott Huntsman; Deborah A. Nickerson; Soren Germer; Michael C. Zody; Gonçalo Abecasis; Hyun Min Kang; Kenneth M. Rice; Rajesh Kumar; Sam Oh; Jose Rodriguez-Santana; Esteban G. Burchard; Max A. Seibold
Title: Type 2 and interferon inflammation strongly regulate SARS-CoV-2 related gene expression in the airway epithelium Document date: 2020_4_10
ID: mj8ebo7i_12_1
Snippet: matory endotype ultimately protects against or 459 exacerbates COVID-19 illness. As mentioned above, we note that measurement of 460 blood eosinophil levels could be used as an informative and more accessible (albeit less 461 powerful) proxy for investigating the association between airway T2 inflammation and 462 outcomes of COVID-19. Moreover, given the higher frequency of T2 inflammation 463 among asthmatic subjects, this population should be m.....
Document: matory endotype ultimately protects against or 459 exacerbates COVID-19 illness. As mentioned above, we note that measurement of 460 blood eosinophil levels could be used as an informative and more accessible (albeit less 461 powerful) proxy for investigating the association between airway T2 inflammation and 462 outcomes of COVID-19. Moreover, given the higher frequency of T2 inflammation 463 among asthmatic subjects, this population should be monitored especially closely given The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.09.034454 doi: bioRxiv preprint In addition to a strong negative influence of T2 inflammation on ACE2 expression in the 468 airway, we found an equally strong positive influence of respiratory virus infections on 469 levels of this gene. Network analysis placed ACE2 within an interferon viral response 470 network suggesting that these cytokines are a driving force behind ACE2 upregulation. 471
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