Science News looks at interleukin-13, an immune-system protein linked with allergies that make it hard to breathe – and make it hard for the SARS-CoV-2 virus to gain a foothold in your lungs:
But it wasn’t clear how IL-13 was protecting people with allergic asthma from SARS-CoV-2, the coronavirus that causes COVID-19. To find out, pathophysiologist Camille Ehre of the University of North Carolina School of Medicine in Chapel Hill and colleagues grew cells from the lining of the airways from six lung donors. Some of the cells were treated with IL-13 to mimic allergic asthma. Then the researchers infected some of the cells with SARS-CoV-2.
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Uninfected cells grew in lawns resembling lush grasslands, where the tufts of waving fronds are actually hairlike protrusions called cilia, which grow from the tops of airway-lining cells, the team confirmed. Cilia’s motions help move mucus, and anything stuck in the mucus, out of the lungs.
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Cells infected with the coronavirus looked much different. The lush lawn was now slathered in mucus, and bald spots appeared as infected cells died. The doomed cells get squeezed out of the lawn of cilia and inflate like a balloon. The inflation happens partly because chambers called vacuoles inside the infected cells get clogged with viruses.
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When researchers doused the cells with IL-13 before adding the coronavirus, the results were strikingly different.
The lawn of waving cilia atop the treated cells was mostly intact, with far fewer balloons of dying cells rising above the surface. But the fronds didn’t wave as vigorously as in untreated cells. That’s because IL-13 reduces cilia beating, the researchers found. Less active cilia could mean that virus-laden mucus sticks around longer. “That can be a double-edged sword inside the lungs because you want to clear the mucus, but you don’t want to spread it around,” Ehre says.
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All that extra mucus from the treated cells could ensnare viruses and expel them from the lungs before much damage is done. But people with nonallergic asthma and COPD make plenty of mucus too, and they aren’t protected from the virus. So Ehre and colleagues stripped away the mucus to see how the airway cells fared without this phlegmy trap.
Even without the mucus, IL-13 was still protective.
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Examining patterns of gene activity, the team found that IL-13 was also causing cells to make less ACE2, the protein that SARS-CoV-2 commandeers as a gateway into cells. “It makes it much harder for the virus to find its door to enter the cells,” Ehre says.
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You can read more of the IL-13 research here, in the Proceedings of the National Academy of Sciences.