Bradykinin is a proinflammatory protein that participates in the homeostatic control of blood pressure. It induces hypotension (low blood pressure) and vasodilation. Hyaluronic acid is a molecule with a high capacity for retaining water. Findings from a new study suggest that bradykinin and hyaluronic acid work in a synergistic fashion to impair gas exchange in the lungs of people with severe cases of COVID-19.

COVID-19, the disease caused by SAR-CoV-2, can cause severe lung complications, including pneumonia. As COVID-19 pneumonia progresses, the lungs' air sacs fill with fluid. Shortness of breath typically ensues, eventually leading to acute respiratory distress syndrome, a form of lung failure.

The authors of the study analyzed gene expression data from cells in bronchoalveolar lavage fluid samples taken from nine COVID-19-positive patients. They compared the data to those obtained from healthy people.

They noted a critical imbalance in the renin-angiotensin-system, a critical regulator of blood pressure, inflammation, and body fluid homeostasis. This imbalance promoted alterations in the expression of the key components of the system, chiefly an increase in bradykinin receptors. The authors also observed that genes that drive hyaluronic acid synthesis and breakdown were altered in the COVID-19 bronchoalveolar lavage fluid samples from the COVID-19 patients. The likely outcome of these changes would be increased bradykinin levels, vascular dilation, vascular permeability, and the formation of a viscous jelly-like substance that would negatively impact gas exchange in the lungs.

These findings point to molecular mechanisms underlying the complications associated with COVID-19 and provides therapeutic intervention possibilities for already-approved pharmaceuticals.

• Link to full study.

• Learn more about COVID-19 in these Q&As featuring Dr. Rhonda Patrick, released April 14 and June 10.