It will take lots more research to see if the fix lasts, to find out if the lungs work as well back inside a body as they do inside a see-through life-support dome in the laboratory. But the study published yesterday has lung specialists hopeful they can boost the number of lungs available for people desperately in need.

"It's a long way from prime time," cautioned Michael Bousamra, lung-transplant chief at Jewish Hospital in Louisville, Ky., who was not involved in the study. But, he added, "this approach has the potential to change the way we do things."

Only about 15 percent of the lungs now provided from otherwise good organ donors are usable for transplant.

The problem often is not that the lungs were diseased. Rather, the delicate airways are damaged as doctors try to keep the donor alive, or brain death causes massive inflammation that triggers further damage. And transplanted lungs are vulnerable to a cascade of inflammation in the first three days after surgery.

In fact, the five-year survival of lung-transplant recipients is barely 50 percent, worse than for heart, liver, or kidney recipients.

The new research, from Toronto's University Health Network, aims first to save donated lungs that would be discarded - and if that works, it might help fend off post-transplant damage, too.

The key: a gene that produces a substance called interleukin-10. Among IL-10's many jobs is tamping down inflammation from the very molecules most prone to damage lungs. But when lungs are donated, they are quickly put on ice to stop tissue deterioration, and that keeps whatever IL-10 remains from working.

So Shaf Keshavjee, the University Health Network's lung-transplant chief, devised a two-part fix: First, create a body-temperature chamber that will keep the lungs alive outside the body. His team made a protective dome to house the lungs; a solution of oxygen and nutrients is pumped into them, mimicking the body without the blood.

Second, insert a gene into those lungs that will quickly produce high levels of IL-10 and reverse inflammation.

His team reports success in yesterday's journal Science Translational Medicine. It stuck the IL-10 gene into an adenovirus, from the family of cold viruses, so it would be taken up by lung cells.

"The beauty of what we're doing here," Keshavjee said, "is we're transducing the cells in the lung to become little IL-10 factories. It's personalized medicine for the organ, if you will."