@article {Chuang00174-2020, author = {Hsiao-Chi Chuang and Yi-Ying Chen and Ta-Chih Hsiao and Hsiu-Chu Chou and Han-Pin Kuo and Po-Hao Feng and Shu-Chuan Ho and Jen-Kun Chen and Kai-Jen Chuang and Kang-Yun Lee}, title = {Alteration in angiotensin-converting enzyme 2 by PM1 during the development of emphysema in rats}, volume = {6}, number = {4}, elocation-id = {00174-2020}, year = {2020}, doi = {10.1183/23120541.00174-2020}, publisher = {European Respiratory Society}, abstract = {Introduction Angiotensin-converting enzyme 2 (ACE2) provides an adhesion site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Patients with COPD could have severe outcomes after SARS-CoV-2 infection. The objective of this study was to investigate ACE2 regulation by air pollution during the development of COPD.Methods Sprague Dawley rats were exposed to unconcentrated traffic-related air pollution for 3 and 6 months. We examined lung injury markers, oxidative stress, inflammation, emphysema, ACE2 and angiotensin II receptor type 1 (AT1) and 2 (AT2) in the lungs after exposure.Results Lung injury occurred due to an increase in permeability and lactate dehydrogenase cytotoxicity was observed after 6 months of exposure to fine particulate matter of \<1 μm in aerodynamic diameter (PM1). An α1-antitrypsin deficiency and neutrophil elastase production with emphysema development were observed after 6 months of PM1 exposure. 8-isoprostane and interleukin-6 were increased after 3 and 6 months of PM1 exposure. Caspase-3 was increased after exposure to PM1 for 6 months. Upregulation of ACE2 was found after 3 months of PM1 exposure; however, ACE2 had decreased by 6 months of PM1 exposure. AT1 and AT2 had significantly decreased after exposure to PM1 for 6 months. Furthermore, smooth muscle hypertrophy had occurred after 6 months of PM1 exposure.Conclusions In conclusion, short-term exposure to PM1 increased the ACE2 overexpression in lungs. Long-term exposure to PM1 decreased the ACE2 overexpression in emphysema. Air pollution may be a risk for SARS-CoV-2 adhesion during the development of COPD.Short-term exposure to PM1 increases ACE2 overexpression in lungs. Long-term exposure to PM1 decreases the ACE2 overexpression in emphysema. Air pollution may be a risk for $\#$SARSCoV2 adhesion during the development of COPD. https://bit.ly/2Vfykur}, URL = {https://openres.ersjournals.com/content/6/4/00174-2020}, eprint = {https://openres.ersjournals.com/content/6/4/00174-2020.full.pdf}, journal = {ERJ Open Research} }