COPD is an often fatal condition where the lungs are damaged and airflow is impeded making it difficult to breathe. There is currently no cure for COPD although there are treatments to help ease symptoms.
The development of COPD occurs over many years mostly occurring in people aged 45 and over.
At Centenary our research into COPD is looking at the impact of inflammation and potential treatments around a number of areas. These include fibrotic tissue remodelling, molecular impacts of infections, oxidative stress on the lungs and the role of our diet and microbiome.
Inflammation is a critical driver of many disease features of COPD including fibrosis, emphysema, impaired gas exchange and severe breathing difficulties. There are many different processes that contribute to inflammation (inflammatory epithelial cells, macrophages, mast cells, complement system, inflammasomes) that we have high level expertise in. We have specific tools that we can use to define their specific roles and which are most important in driving COPD.
Oxidative stress and immunometabolism
These processes are major drivers of disease pathology in COPD and other chronic respiratory diseases. We have several new compounds, some naturally derived, that target and suppress these factors at their source. This source is damaged mitochondria that become dysfunctional when exposed to cigarette and bushfire smoke, air pollution and other environmental challenges.
Microbiomes / metabolites / diet
We are also microbiologists and have extensive expertise in analysing the microbial populations (the microbiome) and the factors that they produce (metabolites) in the lung and the gut and examining how they drive or protect against COPD and can be modified with specific dietary components.
This is the study of processes that modify DNA without affecting its sequence. We are working out how these change in COPD (microRNA, acetylation, methylation) and how they change the activity of diseases and drive disease features.
Fibrosis is the deposition of collagen in lung tissue leading to hardening and damage of the airways and alveoli. It is a major feature of COPD but current therapies have little effect against it. We have advanced knowledge of the role of inflammation and how it drives fibrosis in the lung.
We are performing several studies where we perform high throughput analysis of different groups of factors (mRNA, microRNA, proteins, phosphoproteins, lipids, microbiomes, metabolomes, acetylation, methylation). We can integrate all of these analyses together to obtain a more holistic view of how COPD develops and progresses, and we can also identify pivotal factors that control different parts of the disease and may be more effective targets.
We can use our expertise in each of these areas to develop new therapies to prevent or reverse the development of disease features in COPD and other related diseases such as asthma, pulmonary fibrosis, COVID-19 and lung cancer.
Professor Phil Hansbro, Director of the Centenary UTS Centre for Inflammation leads this research.
COPD was the 5th leading cause of death in Australia in 2018.1 AIHW
Around 1 in 7 Australians aged 40 years and over have some form of COPD. 1 AIHW
Many people with COPD symptoms do not know they have the condition.1 AIHW
COPD is estimated to have cost the Australian health system $977 million in 2015-16.2 AIHW
What are COPD symptoms?
COPD is formally defined by abnormal lung function and clinical testing is required to accurately diagnose it.
The symptoms of COPD include:
- sputum production
- dyspnoea (difficult or laboured breathing)
COPD symptoms often don’t appear until significant lung damage has occurred, which usually worsens over time. However, it can be difficult to distinguish COPD from asthma because the symptoms of both conditions can be similar.