Abstract | INTRODUCTION: METHODS: 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.
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Authors | Hsiao-Chi Chuang, Yi-Ying Chen, Ta-Chih Hsiao, Hsiu-Chu Chou, Han-Pin Kuo, Po-Hao Feng, Shu-Chuan Ho, Jen-Kun Chen, Kai-Jen Chuang, Kang-Yun Lee |
Journal | ERJ open research
(ERJ Open Res)
Vol. 6
Issue 4
(Oct 2020)
ISSN: 2312-0541 [Print] England |
PMID | 33043050
(Publication Type: Journal Article)
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Copyright | Copyright ©ERS 2020. |