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Wednesday, November 30, 2022

Some types of asthma protect against severe COVID-19, and we may finally know why

When the COVID-19 pandemic first began, people with chronic lung conditions like asthma were concerned about the disease, which was especially serious for them. However, it appears that people with certain types of asthma are doing better than expected – and we may finally understand why.

Population-based studies in Australia, the UK and Europe and the United States have so far found no evidence that asthma causes severe symptoms of COVID-19.

In fact, it’s quite the opposite. In general, people with allergic asthma are less likely to actually get sick after catching SARS-CoV-2; This is in contrast to people with other lung conditions such as emphysema, which are more likely to have severe symptoms.

So what sets asthma patients apart? Researchers at the University of North Carolina at Chapel Hill think they have finally figured it out.

To research this, the team used cell culture from the human respiratory tract. To mimic the airways of people with asthma, they treated some samples with a small protein known to be more prevalent in asthma, called interleukin-13 (IL-13). One of the reasons for its presence in patients with asthma is the acceleration of mucus production beyond healthy levels.

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Then, they infected the cell cultures with SARS-CoV-2. In IL-13-treated cells, the coronavirus showed trouble invading the cell in order to replicate and spread copies of itself. In untreated cells, meanwhile, there were many more infections.

“We knew there must have been a biomechanical reason that people with allergic asthma were more protected from severe disease,” says UNC biochemist Camille Ehre.

“Our research team discovered several important cellular changes specifically caused by IL-13, leading us to conclude that IL-13 plays a unique role in protecting against SARS-CoV-2 infection in certain patient populations. “

When respiratory cells and viruses were observed interacting under an electron microscope, Ehre and colleagues observed that IL-13 treatment significantly decreased the number of infected cells, while increasing the mucus that produced these cells. happened.

Even when the mucus was removed, however, the cells showed some degree of protection against the invading coronavirus.

RNA-sequencing further confirmed that the presence of IL-13 in cell culture was upregulating genes associated with antiviral properties, while downregulating the expression of cell receptors that are known to attach to coronaviruses, like ACE2 .

In untreated respiratory cells, these receptors allow a coronavirus to invade relatively easily. If a cell was indeed infected, the researchers observed that it was more likely to move away from the surface of the airways, allowing it to fall deeper into the lungs, spreading the infection.

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“In conclusion, the acute viral and cell shedding caused by SARS-CoV-2 infection was attenuated by IL-13, which affected viral entry, replication and spread,” conclude the authors.

Unfortunately IL-13 cannot be used as a treatment by itself. It is part of the immune response, which means it can trigger inflammation in the patient’s airways.

But it’s still important to understand the finer details of what’s happening in the lungs. By comparing cells that mimic the asthmatic airway to healthy airway cells, scientists have shed light on some of the underlying mechanisms behind severe COVID-19 cases.

In the future, therapeutic drugs may help target certain sites that appear to be more involved in severe symptoms.

“We think this research further shows how important it is to treat SARS-CoV-2 infection as early as possible,” says Ehre.

“And it shows how important the specific mechanisms involving ACE2 and IL-13 are, as we do our best to protect patients from developing serious infections.”

The study was published in PNAS,

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