scholarly journals Cigarette Smoke Exposure Alters Bacterial-Host Interactions in the Respiratory Tract to Promote Disease

2017 ◽  
Vol 3 (3) ◽  
Author(s):  
Pamela Shen ◽  
Martin R. Stämpfli
Keyword(s):  
Respiratory Tract ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Bacterial Host ◽  
Host Interactions

scholarly journals Cigarette Smoke Exposure and Inflammatory Signaling Increase the Expression of the SARS-CoV-2 Receptor ACE2 in the Respiratory Tract

2020 ◽  
Vol 53 (5) ◽  
pp. 514-529.e3 ◽  
Author(s):  
Joan C. Smith ◽  
Erin L. Sausville ◽  
Vishruth Girish ◽  
Monet Lou Yuan ◽  
Anand Vasudevan ◽  
...  
Keyword(s):  
Respiratory Tract ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Inflammatory Signaling

Cigarette smoke exposure attenuates the induction of antigen-specific IgA in the murine upper respiratory tract

2021 ◽  
Author(s):  
Joshua J. C. McGrath ◽  
Danya Thayaparan ◽  
Steven P. Cass ◽  
Jonathan P. Mapletoft ◽  
Peter Y. F. Zeng ◽  
...  
Keyword(s):  
Respiratory Tract ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Upper Respiratory Tract ◽  
Upper Respiratory

scholarly journals Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tract

2020 ◽  
Author(s):  
Joan C. Smith ◽  
Erin L. Sausville ◽  
Vishruth Girish ◽  
Monet Lou Yuan ◽  
Kristen M. John ◽  
...  
Keyword(s):  
Respiratory Tract ◽  
Cigarette Smoke ◽  
Viral Infections ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Secretory Cells ◽  
Sequencing Data ◽  
Inflammatory Signaling ◽  
Human Lungs ◽  
Quitting Smoking

AbstractThe factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of Angiotensin Converting Enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression. In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, we demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, our work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive-feedback loops that increase ACE2 levels and facilitate viral dissemination.

Cigarette smoke exposure induces substantial changes in the airway epithelium of a Drosophila COPD model

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
M Thiedmann ◽  
R Prange ◽  
A Bhandari ◽  
K Kallsen ◽  
C Fink ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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