Cigarette Smoke Exposure and Inflammatory Signaling Increase the Expression of the SARS-CoV-2 Receptor ACE2 in the Respiratory Tract
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SciScore for 10.1101/2020.03.28.013672: (What is this?)
Please note, not all rigor criteria are appropriate for all manuscripts.
Table 1: Rigor
Institutional Review Board Statement not detected. Randomization not detected. Blinding not detected. Power Analysis not detected. Sex as a biological variable not detected. Table 2: Resources
No key resources detected.
Results from OddPub: Thank you for sharing your code.
Results from LimitationRecognizer: We detected the following sentences addressing limitations in the study:Alternately, ACE2 may be expressed in mesenchymal or other lineages within the lung, and our inability to detect it may be a limitation of the single-cell samples that we analyzed. Nonetheless, by examining datasets from both mice and humans, and by including cells collected from bronchial brushing, we demonstrated consistently high …
SciScore for 10.1101/2020.03.28.013672: (What is this?)
Please note, not all rigor criteria are appropriate for all manuscripts.
Table 1: Rigor
Institutional Review Board Statement not detected. Randomization not detected. Blinding not detected. Power Analysis not detected. Sex as a biological variable not detected. Table 2: Resources
No key resources detected.
Results from OddPub: Thank you for sharing your code.
Results from LimitationRecognizer: We detected the following sentences addressing limitations in the study:Alternately, ACE2 may be expressed in mesenchymal or other lineages within the lung, and our inability to detect it may be a limitation of the single-cell samples that we analyzed. Nonetheless, by examining datasets from both mice and humans, and by including cells collected from bronchial brushing, we demonstrated consistently high levels of ACE2 transcripts in the secretory cells that participate in mucociliary clearance48. As these cells line the upper respiratory tract, they may represent the initial site of coronavirus infections, followed by an eventual spread and migration into the alveoli. Cigarette smoke has a profound impact on the lungs of chronic smokers. Notably, prolonged smoke exposure triggers secretory cell hyperplasia, thereby increasing the production of mucous in the respiratory tract64–66. We found that this smoking-induced expansion of secretory cells also causes an increase in ACE2 levels, as smoking doubled the number of cells co-expressing ACE2 and MUC5AC. Additionally, consistent with a recent report122, we found that ACE2 is an interferon-regulated gene, and is over-expressed in lung epithelial cells following viral infection or interferon treatment. Lung damage and inflammation caused by smoking could also contribute to ACE2 upregulation. Additionally, we speculate that the interferon-dependent upregulation of ACE2 could create a positive-feedback loop for SARS-CoV-2 infections. That is, interferon secretion following an initial infection could inc...
Results from TrialIdentifier: No clinical trial numbers were referenced.
Results from Barzooka: We did not find any issues relating to the usage of bar graphs.
Results from JetFighter: We did not find any issues relating to colormaps.
Results from rtransparent:- Thank you for including a conflict of interest statement. Authors are encouraged to include this statement when submitting to a journal.
- No funding statement was detected.
- No protocol registration statement was detected.
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