Australian and American researchers have discovered a protein that inhibits the lungs from repairing itself from smoke related diseases, in a breakthrough that could lead to a potential new treatment for patients.

A group of international researchers from the University of Melbourne, Royal Melbourne Hospital and the Brigham and Women's Hospital Harvard Medical School in the U.S. discovered that the protein SAA plays a key role in chronic inflammation of the lungs and inhibits the natural healing process of the lungs even after the patient has stopped smoking. The study looked at 100 Melbourne patients and found that the protein SAA played a key role in inflaming their lungs, caused breathing difficulties and impaired the lungs repair process.

Professor Gary Anderson, head of the Melbourne University lung disease research laboratory, said that the study could improve the treatment of Chronic Obstructive Pulmonary Disease (COPD) including emphysema.

"It has the potential to dramatically improve the lives of many people suffering these conditions and reduce the huge burden of health and hospital costs associated with their treatment," he said.

COPD is a progressive disease caused by excessive smoking. Common symptoms include breathlessness, coughing, fatigue and increased susceptibility to chest infections. According to the Australian Lung Foundation there are 2.1 million Australians suffering from COPD. The numbers are expected to rise to 4.5 million by 2050. Of the 2.1 million Australians who have some form of COPD, 1.2 million have Stage II to IV COPD at which symptoms are already affecting their lives.

The study is significant because it proved that SAA which was previously known as being produced in the liver to fight infection, served to aggravate the condition when it appeared in the lungs of patients with COPD. Anderson said the finding explained why steroids didn't work with COPD even though they were effective in battling other lung diseases like asthma.

''Steroid treatments work by turning off the production of inflammatory substances, but our finding reveals they fail to block the production of SAA and hence inflammation in the lung," he said. ''We believe SAA plays a critical role in why steroids are much less effective in treating COPD.''

The discovery could lead to a new dual treatment which would switch off the SAA function in the lungs and then adding a synthetic agent in the lungs that would boost natural healing. The synthetic agent is already being developed in the U.S.

Professor Anderson said that even if the treatment would reduce the damage from smoking, the best treatment is not smoking at all.

"This is not a golden ticket to smoke," he said. "We are hopeful the combined treatment will assist patients of all stages of COPD, particularly those in stage four with constant hospital visits, to improve their quality of life, but it would not cure disease."