scholarly journals Traffic-derived particulate matter and angiotensin-converting enzyme 2 expression in human airway epithelial cells

2020 ◽  
Author(s):  
L Miyashita ◽  
G Foley ◽  
S Semple ◽  
J Grigg
Keyword(s):  
Particulate Matter ◽  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Cigarette Smoke ◽  
A549 Cells ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Human Airway

AbstractBackgroundThe mechanism for the association between traffic-derived particulate matter less than 10 microns (PM10) and cases of COVID-19 disease reported in epidemiological studies is unknown. To infect cells, the spike protein of SARS-CoV-2 interacts with angiotensin-converting enzyme 2 (ACE2) on host airway cells. Increased ACE2 expression in lower airway cells in active smokers, suggests a potential mechanism whereby PM10 increases vulnerability to COVID-19 disease.ObjectiveTo assess the effect of traffic-derived PM10 on human airway epithelial cell ACE2 expression in vitro.MethodsPM10 was collected from Marylebone Road (London) using a kerbside impactor. A549 and human primary nasal epithelial cells were cultured with PM10 for 2 h, and ACE2 expression (median fluorescent intensity; MFI) assessed by flow cytometry. We included cigarette smoke extract as a putative positive control. Data were analysed by either Mann-Whitney test, or Kruskal-Wallis with Dunn’s multiple comparisons test.ResultsPM10 at 10 μg/mL, and 20 μg/mL increased ACE2 expression in A549 cells (P<0.05, 0.01 vs. medium control, respectively). Experiments using a single PM10 concentration (10 μg/mL), found increased ACE2 expression in both A549 cells (control vs. PM10, median (IQR) MFI; 470 (0.1 to 1114) vs 6217 (5071 to 8506), P<0.01), and in human primary epithelial cells (0 (0 to 591) vs. 4000 (2610 to 7853), P<0.05). Culture of A549 cells with 5% cigarette smoke extract increased ACE2 expression (n=4, 0 (0 to 28) vs. 9088 (7557 to 15831, P<0.05).ConclusionTraffic-related PM10 increases the expression of the receptor for SARS-CoV-2 in human respiratory epithelial cells.

Regulation of the Expression of SARS-CoV-2 Receptor Angiotensin-Converting Enzyme 2 in Nasal Mucosa

2021 ◽  
pp. 194589242110277
Author(s):  
Tetsuji Takabayashi ◽  
Kanako Yoshida ◽  
Yoshimasa Imoto ◽  
Robert P. Schleimer ◽  
Shigeharu Fujieda
Keyword(s):  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Nasal Mucosa ◽  
Japanese Cedar ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Japanese Cedar Pollen ◽  
Cedar Pollen

Background Coronavirus disease 2019 (COVID-19) has caused a global pandemic. Higher expression of the virus receptor angiotensin-converting enzyme 2 (ACE2) in the nasal mucosa may be associated with high transmissibility and asymptomatic infection. In COVID-19, the elucidation of the determinants of ACE2 expression at nasal tissue level is crucial. The development of strategies to downregulate ACE2 expression in nasal epithelial cells might reduce transmission and be useful as a novel therapeutic approach. Objective To verify ACE2 expression in the nasal mucosa of patients with seasonal allergic rhinitis induced by Japanese cedar pollen (SAR-JCP) and chronic rhinosinusitis with nasal polyp (CRSwNP) and to examine the effects of short-chain fatty acids (SCFAs) on ACE2 expression in airway epithelial cells. Methods We assessed ACE2 expression in the nasal mucosa of control subjects, patients with SAR-JCP, and those with CRSwNP using real-time polymerase chain reaction. We also quantified ACE2 gene expression in cultured airway epithelial cells. Results Although ACE2 expression was greatly increased in a few patients with SAR-JCP during the Japanese cedar pollen season, mean levels were not significantly increased. ACE2 mRNA expression was significantly decreased in nasal polyp tissue from patients with chronic rhinosinusitis compared with the expression in that from control subjects. SCFAs generated by gastrointestinal microbiota significantly reduced resting ACE2 expression in cultured airway epithelial cells. SCFAs also significantly suppressed the dsRNA-dependent upregulation of ACE2 expression in airway epithelial cells. Conclusion Inflammatory endotype affects ACE2 expression in the nasal mucosa and influences susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In particular, type 2 inflammation could downregulate ACE2 expression in the nasal mucosa and reduces susceptibility to SARS-CoV-2 in patients with CRSwNP. Although in vivo experiments are required, administration of SCFAs to the nasal cavity might be worthy of consideration as a preventative or therapeutic strategy for the early-stage COVID-19.

scholarly journals Estrogen regulates the expression of SARS-CoV-2 receptor ACE2 in differentiated airway epithelial cells

2020 ◽  
Vol 318 (6) ◽  
pp. L1280-L1281 ◽  
Author(s):  
Kimberly E. Stelzig ◽  
Fabrizio Canepa-Escaro ◽  
Marta Schiliro ◽  
Sergejs Berdnikovs ◽  
Y. S. Prakash ◽  
...  
Keyword(s):  
Sexual Dimorphism ◽  
Epithelial Cells ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Sex Steroids ◽  
Airway Epithelial Cells ◽  
Cell Entry ◽  
Airway Epithelial ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

There is marked sexual dimorphism in the current coronavirus disease 2019 (COVID-19) pandemic. Here we report that estrogen can regulate the expression of angiotensin-converting enzyme 2 (ACE2), a key component for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cell entry, in differentiated airway epithelial cells. Further studies are required to elucidate the mechanisms by which sex steroids regulate SARS-CoV-2 infectivity.

scholarly journals Identification of the SARS-CoV-2 Entry Receptor ACE2 as a Direct Target for Transcriptional Repression by Miz1

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Yang ◽  
Edith A. Perez ◽  
Changchun Hou ◽  
Pin Zhang ◽  
Michelle Van Scoyk ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Cigarette Smoke ◽  
Lung Epithelial Cells ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Copd Patients ◽  
Lung Epithelial

Multiple lines of evidence have demonstrated that cigarette smoke or Chronic Obstructive Pulmonary Disease upregulates angiotensin-converting enzyme 2, the cellular receptor for the entry of the severe acute respiratory syndrome coronavirus 2, which predisposes individuals to develop severe Coronavirus disease 2019. The reason for this observation is unknown. We recently reported that the loss of function of Miz1 in the lung epithelium in mice leads to a spontaneous COPD-like phenotype, associated with upregulation of angiotensin-converting enzyme 2. We also reported that cigarette smoke exposure downregulates Miz1 in lung epithelial cells and in mice, and Miz1 is also downregulated in the lungs of COPD patients. Here, we provide further evidence that Miz1 directly binds to and represses the promoter of angiotensin-converting enzyme 2 in mouse and human lung epithelial cells. Our data provide a potential molecular mechanism for the upregulation of angiotensin-converting enzyme 2 observed in smokers and COPD patients, with implication in severe Coronavirus disease 2019.

Cigarette smoke extract reduces VEGF in primary human airway epithelial cells

2009 ◽  
Vol 33 (4) ◽  
pp. 835-843 ◽  
Author(s):  
J. V. Thaikoottathil ◽  
R. J. Martin ◽  
J. Zdunek ◽  
A. Weinberger ◽  
J. G. Rino ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells
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