Author: Bradding, Peter; Richardson, Matthew; Hinks, Timothy S.C.; Howarth, Peter H.; Choy, David F.; Arron, Joseph R.; Wenzel, Sally E.; Siddiqui, Salman
Title: ACE2, TMPRSS2 AND FURIN GENE EXPRESSION IN THE AIRWAYS OF PEOPLE WITH ASTHMA – IMPLICATIONS FOR COVID-19 Cord-id: 806tgnt0 Document date: 2020_5_22
ID: 806tgnt0
Snippet: Abstract To-date, there has not been a clear signal suggesting that asthma or treatment with inhaled steroids are a risk factor for severe COVID-19 disease. We have therefore explored ACE2 receptor mRNA expression, and co-factors for Sars-CoV-2 infectivity (TMPRSS2 and furin) in bronchial brushes and biopsies from people with asthma and healthy controls, and looked for relationships between asthma severity, Th2- and IL-17 dependent gene signatures, and clinical demographics (age, sex). We have l
Document: Abstract To-date, there has not been a clear signal suggesting that asthma or treatment with inhaled steroids are a risk factor for severe COVID-19 disease. We have therefore explored ACE2 receptor mRNA expression, and co-factors for Sars-CoV-2 infectivity (TMPRSS2 and furin) in bronchial brushes and biopsies from people with asthma and healthy controls, and looked for relationships between asthma severity, Th2- and IL-17 dependent gene signatures, and clinical demographics (age, sex). We have looked at a cohort of 356 research participants from previously described studies. The only significant association was a positive correlation between ACE2 and IL-17-dependent gene expression, and an inverse correlation between ACE2 and Th2-cytokine-dependent gene expression. These data suggest that differences in ACE2, TMPRSS2 and furin epithelial and airway gene expression are unlikely to confer enhanced COVID-19 pneumonia risk in patients with asthma across all treatment intensities and severity.
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