Author: Abikenova Ayazhan
Translator: Turarova Aiym
Copy editors: Kigbayeva Kamila, Issabayeva Madina
Data from patients with COVID-19 suggests that smokers are more likely to develop complications. Jason Sheltzer, cancer geneticist in the laboratory ColdSpringHarborLaboratory:
"Our results provide insight into why smokers who develop COVID-19 have poor clinical results. We found that Smoking causes a significant increase in the expression of ACE2, a protein that SARS-CoV-2 uses to enter human cells."
ACE2 (angiotensin-converting enzyme 2) is a regulatory protein that increases the vulnerability of a human cell to the 2003 SARS virus (2003). "Data from experiments on mice showed that higher levels of ACE2 make mice more susceptible to SARS," says Sheltzer. More recent work with SARS-CoV-2 has shown that high expression of human ACE2 in mice infected with COVID-19 leads to a high mortality rate.
In humans, the lungs are one of the sources of ACE2 production. To assess the direct effect of Smoking on ACE2 expression in the lungs, Sheltzer compared the expression of the ACE2 gene from the lung epithelial tissue of people who regularly smoked cigarettes with those who never smoked. According to the results of the experiment, smokers produced 30-55% more ACE2 than their non-Smoking counterparts. These indicators also depended on the frequency of Smoking, with heavy smokers having the highest ACE2 values.
The effect of Smoking on ACE2 may be related to goblet cells in the lungs (cells that produce mucus to moisten and protect the mucous membrane of the respiratory tract) - one of the few types of lung cells that, according to Sheltzer, actively express the ACE2 gene. The rise in ACE2 levels has also been associated with inflammatory lung diseases, COPD (chronic obstructive pulmonary disease) and idiopathic pulmonary fibrosis (a chronic disease caused by scarring of lung tissue), as well as viral infections such as influenza, and increased interferon (an immune system protein that protects against viruses).
Although the effects of cigarette smoke and ACE2 expression are convincing, they are not permanent. Comparing the lungs of current smokers with those who quit smoking at least 12 months ago, Sheltzer found that a significant decrease in ACE2 expression demonstrates that the effect of smoking on ACE2 is reversible. In addition, other studies on the effects of cigarette smoke have shown mixed results. "Cigarette smoke contains hundreds of different chemicals. It is possible that some components (e.g., nicotine) act differently than whole smoke," says Sheltzer.
Even if Sheltzer links the regulation of ACE2 gene expression to smoking, the ACE2 protein can be regulated in other ways not considered in this study. "It can be assumed that having a large number of cells that express ACE2 facilitates the spread of SARS-CoV-2 in the lungs, but we have yet to study much more," - Jason Sheltzer.
Source: https://medicalxpress.com/news/
