Oct. 28 (HealthDay News) -- A new type of gene therapy for injured lungs that were previously rejected for transplantation may increase the number of lungs available for transplant, researchers say.

Successful transplants require healthy lungs, but more than 80 percent of donor lungs are highly inflamed and only mildly functional, which means many of them are rejected by surgeons, according to researchers with the University Health Network in Toronto.

The investigators found that infusion with the regulatory gene IL-10 before transplant can heal damaged donor lungs. This procedure involves placing the lungs in a glass chamber outside the body and keeping them breathing using a perfusion system that continuously pumps a solution of oxygen, proteins and nutrients into the lungs.

The study, published in the Oct. 28 issue of Science Translational Medicine, noted that the current method of preserving donor organs is to keep them on ice. But the new lung perfusion system would enable the lung's cellular machinery to keep working by maintaining the lungs at a normal body temperature, the study authors explained in a news release from the journal's publisher.

In one experiment, pig lungs that underwent IL-10 gene therapy and lung perfusion for 12 hours had better function and less swelling when transplanted into recipient pigs. The researchers also found that this treatment produced similar results in human lungs previously rejected for transplant.

Further investigation showed that IL-10 reduced inflammation, refurbished the alveoli (tiny branching sacs where gas exchange occurs), and improved function in the injured donor lungs.

Another study published in the same issue of the journal identified two types of immune cells that play a major role in the destruction of smokers' lungs.

Smoking-related irritation of the lungs triggers a complex immune response that includes an accumulation of different types of immune cells. An analysis of lung tissue from emphysema patients revealed the normally helpful immune cells called dendritic cells travel to the lung and induce T-helper 1 and T-helper 17 cells to destroy lung tissue and proteins responsible for lung elasticity.

The T-helper 17 cells secrete a protein that triggers a reaction that attracts more dendritic cells to the lungs, leading to a repeat of the destructive cycle, the researchers found.

The findings offer more evidence that emphysema (primarily caused by cigarette smoke) is an autoimmune disease. This line of research may lead to new drugs that can control lung damage, the study authors said.

SOURCE: Science Translational Medicine, news release, Oct. 28, 2009