When the body fights off infection or injury, inflammation is a natural and often helpful response.
But in severe illnesses like sepsis, acute respiratory distress syndrome, or COVID-19, inflammation can spiral out of control.
One dangerous result is blood vessel leakage, where fluid and proteins escape from the bloodstream into surrounding tissues.
This leakage can lead to swelling, organ damage, and, in the worst cases, multi-organ failure and death.
A new study from the University of Oklahoma has identified a protein that plays an important role in this process—and may offer a new way to protect patients.
The protein, known as CD82, appears to make blood vessels more prone to leak during inflammation.
The research, published in Nature Cardiovascular Research, revealed that removing CD82 from blood vessels in animal models significantly reduced leakage.
“CD82 is part of a family of proteins called tetraspanins,” explained Xin Zhang, Ph.D., senior author of the study and professor of biochemistry and physiology at the OU College of Medicine.
“Tetraspanins are already known for their role in forming new blood vessels and advancing cancer, but their role in inflammation has been less clear. Our findings show that CD82 actually promotes leakage during inflammation.”
The team also uncovered how this process works. They found that CD82 interacts with a small pool of cholesterol that sits on the surface of blood vessel cells, known as “accessible cholesterol.”
When CD82 connects with this cholesterol, it sends signals inside the cells that loosen the vessel walls, allowing fluid to leak out.
Importantly, the researchers discovered a potential way to block this effect. By reducing the amount of accessible cholesterol with a statin—a type of drug commonly prescribed to lower cholesterol levels—they were able to make the blood vessel walls stronger and less leaky.
“This suggests that we may be able to repurpose drugs like statins to help stabilize blood vessels when the body is overwhelmed by inflammation,” Zhang said.
“If we can control vascular leakage, we may be able to protect patients from multi-organ failure.”
The findings are still in the early stages, based on preclinical models rather than human trials. More research is needed to confirm whether the same effect can be achieved in patients. Still, the discovery sheds new light on a poorly understood process and points to promising new treatment strategies.
For now, the identification of CD82 as a key driver of blood vessel leakage offers hope that doctors may one day be able to reduce one of the most dangerous complications of severe illness.
By targeting this protein or manipulating cholesterol in vessel walls, therapies could help patients survive conditions that currently carry high risks of organ failure and death.
