Asthma paradox. Since COVID-19 is primarily a respiratory disease, people with chronic respiratory conditions such as asthma were thought to be at greater risk from the coronavirus. But in contrast, epidemiological studies showed that severe COVID patients did not represent asthma patients, apart from minorities. severe asthma (about 5% of asthmatics). A study published on March 30, 2022 PNAS sheds light on this paradox, showing how the weaknesses of patients with allergic asthma have become strengths during the pandemic.
Asthma patients protected from many obstacles
,We knew there had to be a biomechanistic reason that could explain why some asthma patients seemed to be safe from severe COVID.”, reveals Camille Ehre, researcher at the University of North Carolina at Chapel Hill (USA) and study author in a sent, All that was left was to find him. More specifically, this protection appears to be specific to people with allergic asthma. It is triggered in the presence of allergens such as pollen or mold, which activate the production of cytokines and mucin in the patient’s lungs. Specifically the mucin MUC5AC, which is secreted by some lung cells during respiratory infections, and which is produced in excess in patients with asthma. This mucin production is regulated by interleukin 13 (IL-13), an anti-inflammatory cytokine that is overexpressed in patients with asthma.
First mucin barrier that blocks virus
Researchers mimicked asthma with lung cells treated with this interleukin 13, then infected them with the SARS-CoV-2 coronavirus. Thus, they have shown that protection against COVID is played at multiple levels. First, the excessive production of mucin created a physical barrier that protected these cells to some degree from infection. In untreated cells, mucin secretion also increased after infection, but these cells were quickly overwhelmed and the amount of mucin was not sufficient to combat virus multiplication.
second barrier by removing the entrances to cells
But this obstacle was not the only one. Because even cells where production of the mucin MUC5AC was inhibited, treatment with interleukin showed a lower viral load. The second barrier was the reduced access of lung cells to the coronavirus, as this cytokine reduced production of the ACE-2 receptor, the virus’s entry point into our cells. Finally, the treated lung cells produced fewer SARS-CoV-2 virions after infection, thus protecting the surrounding cells. ,It is the release of the virus into the lungs that gives the coronavirus its high transmission efficiency and appears to enhance its ability to infect the deeper tissues of the lungs.Camille Ehre explains.
Additional constraints to clear
Other mechanisms may participate in this protection, as the authors observed that the expression of other genes was increased by treatment with the interleukin IL-13. Together, all of these cellular changes resulted in a significant reduction of virus entry into lung cells, replication and spread to other cells. ,This study demonstrates the importance of some specific mechanisms, including the expression of IL-13, and how this can be used to protect patients and prevent them from developing severe forms of COVID-19.”, summarizes the researcher. These results also show how important it will be to treat coronavirus infections as early as possible, before lung cells are overwhelmed by infection.
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