A molecular biologist at Cold Spring Harbor Laboratory, Jason Sheltzer, and his partner, Joan Smith, a software engineer from Google, have been pondering about how the expression of the enzyme ACE2 might have caused different factors on how the coronavirus expressed itself in different people.
Put merely, ACE2 plays a vital role in a biochemical pathway responsible for regulating blood pressure, promoting wound healing, and inflammation. It stands for angiotensin-converting enzyme 2 and is a protein that lies on the surface of many types of cells in the human body. These included the lining in the heart, lungs, intestines, and inside the nose.
Initially, the two, along with other scientists, have thought that the more ACE2 a person had, the more susceptible they were to contracting COVID-19. However, later on, studies have continuously shown that women and men produced similar amounts of ACE2 inside their lung cells.
Furthermore, there were no significant differences between young adults and older ones, as well. Studies revealed that aging didn't change ACE2 levels in any way. However, when it came to smokers, a completely different observation was seen.
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Smoking Drives ACE2 to Increase
In a study by Sheltzer and his colleagues, they found out that secretory goblet cells caused a considerable spike in ACE2. The goblet cells primarily produce mucus to coat the inner layers of the respiratory tract. The team discovered that the more people smoked, the more goblet cells aggregated.
Furthermore, the gathering of the cells was a mechanism to trap chemicals before they could damage surrounding tissues. The findings of the study were published in the clinical journal Developmental Cell on May 16, 2020.
To add up to their hypothesis, another study from the University of British Columbia found that the cells of patients with chronic obstructive pulmonary disease, as well as smokers, produced more ACE2.
However, to fully understand if the link between the two is causative, further studies would need to be conducted. Meanwhile, Scheltzer's team is preparing for more studies involving smokers and SARS-CoV-2.
Manipulation of ACE2 Through Drugs
Scientists have tried to make sense of how ACE2 made a difference between healthy individuals and those with asthma. Although not much was seen, researchers have noted that asthmatic patients who use steroid inhalers had significantly less ACE2. The study published in April can be found in the American Journal of Respiratory and Critical Care Medicine.
According to Michael Peters, one of the authors of the study, the data they collected suggests that inhaled corticosteroids could be a major reason why asthma hasn't arisen as a big risk factor for COVID-19. Furthermore, doctors in China also used steroids to keep inflammation down when treating severe cases of COVID-19.
Additionally, some researchers have also noticed a trend of having hypertension in many coronavirus patients. To lower the blood pressure, patients were given two classes of medications known to increase levels of ACE2.
The two drug classifications, angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors, then prompted health professionals around the world to warn the millions of people using the drug of an increased risk of catching COVID-19 associated with drug use from both classifications.
