In a research published in the European Respiratory Journal, researchers said the drug target is an enzyme known as mast cell chymase-1 (CMA1), as inhibiting the equivalent enzyme in mice was shown to provide protection in experimental models of COPD.
In the study, researchers discovered elevated CMA1 levels in the lung tissues of patients with severe COPD, the CMA1 levels were approximately double of that found in the lung tissue of mild-COPD patients and healthy individuals.
Subsequent investigation also confirmed that mMCP5 in mice, an enzyme equivalent of CMA1, plays a pivotal role in COPD. Mice with deficient mMCP5 levels were protected against cigarette smoke-induced inflammation, macrophage accumulation, airway remodelling, emphysema and impaired lung function in experimental COPD.
"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 Gang Liu, the study's lead author and researcher at the Centenary UTS Center for Inflammation.
Researchers said COPD was caused by cigarette smoke, air pollution, bushfire smoke and other particulate matter. It subsequently impairs lung function over time and leads to breathing difficulties which may then turn fatal.
"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," added Phil Hansbro, the study's senior author and director of the Centenary UTS Center for Inflammation.
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