Australian researchers identify new drug target for inflammatory lung disease

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Australian researchers have identified a new drug target for the treatment and prevention of chronic obstructive pulmonary disease (COPD).

The researchers at Centenary Institute and the University of Technology Sydney say the drug target is an enzyme known as mast cell chymase-1 (CMA1).

They said CMA1 was found to actively promote and progress the development of COPD. According to the researchers, CMA1 could provide a new therapeutic approach to tackling the inflammatory lung disease that causes airway blockage and that makes it difficult to breathe.

Dr Gang Liu, the study’s lead author and researcher at the Centenary UTS Centre for Inflammation, said, “Over time the lungs breathe in toxic material and become inflamed. Lung function is subsequently impaired leading to breathing difficulties which can then turn fatal.”

The researchers discovered elevated CMA1 levels in the lung tissues of patients with severe COPD – the CMA1 levels were approximately double that found in the lung tissue of mild-COPD patients and healthy individuals.

“CMA1 induces macrophages (a type of white blood cell) to release pro-inflammatory cytokines in the lung. It’s this increased inflammation that can drive the development of COPD and poor outcomes for patients,” said Dr Liu.

“We were able to show in experimental COPD, that inhibiting mMCP5 provided protection against inflammation and macrophage accumulation, harmful structural changes of the lung, emphysema and impaired lung function.”

Professor Phil Hansbro, the study’s senior author and Director of the Centenary UTS Centre for Inflammation said the team’s research offered up a new therapeutic target to help combat COPD.

“There is currently no cure for COPD and effective therapies to treat and manage the disease are urgently needed. Our study suggests that developing new drugs to inhibit CMA1 and reduce cytokine inflammation may be a novel treatment for this devastating disease that affects so many lives,” said Professor Hansbro.