Is a Bradykinin Storm Brewing in COVID-19?

Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. Clinical trials of inhibitors are putting this hypothesis to the test.

Written byAlakananda Dasgupta
| 5 min read
bradykinin kinin cascade ras covid-19 sars-cov-2 dabk cytokines macrophage edema fluid lung leaky blood vessel

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ABOVE: A hyperactive bradykinin system permits fluid, shown in yellow, to leak out of a blood vessel and allows immune cells, shown in purple, to squeeze out as well.
JASON SMITH/ORNL, US DEPARTMENT OF ENERGY

On a Sunday afternoon in mid-April this year, Daniel Jacobson, a computational systems biologist at Oak Ridge National Laboratory in Tennessee, was looking at gene expression data from the lung fluid of COVID-19 patients on his computer screen when he spotted something striking—the expression of genes for key enzymes in the renin-angiotensin system (RAS), involved in blood pressure regulation and fluid balance, was askew.

Jacobson followed this abnormal RAS in the lung fluid samples to the kinin cascade, an inflammatory pathway that is tightly regulated by the RAS. He found that the kinin system—in which a key peptide, bradykinin, causes blood vessels to leak and fluid to accumulate in tissues and organs—was thrown out of balance ...

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  • alakananda dasgupta

    Alakananda Dasgupta is a freelance science journalist based in New Delhi, India, who contributes to The Scientist. She is a medical doctor and a pathologist by training. In 2018, she combined her interests in science and writing and became a science writer. She has done research previously in the field of immunology and is currently writing a book on the subject.

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