An international team including Australian researchers has identified a potential new approach for treating chronic obstructive pulmonary disease (COPD) – a group of diseases that includes emphysema and chronic bronchitis.
In COPD airway inflammation, blockage, and lung damage causes airflow blockage making it difficult to breathe. According to the World Health Organization (WHO) COPD is the third leading cause of death worldwide, causing 3.23 million deaths in 2019.
Lung Foundation Australia says: “Around 1 in 13 Australians aged 40 years and over have some form of COPD however around half of these people living with COPD symptoms do not know they have the condition. Indigenous Australians are 2.5 times more likely to have COPD than non-Indigenous Australians. About 20% of people with COPD also have asthma. COPD is not contagious.
Existing treatments and lifestyle changes like quitting smoking, can slow the progression of the disease but cannot reverse the damage. There is currently no cure.
Now, a new study in the European Respiratory Journal has found that there are increased levels of an enzyme called Receptor-interacting protein kinase 1 (RIPK1) in the lungs of people suffering from COPD.
Inhibiting this enzyme helped protect against COPD in mouse models and may represents a new approach for treatment in humans.
According to co-senior author Professor Phil Hansbro, Director of the Centenary UTS Centre for Inflammation at the University of Technology Sydney, while smoking is the primary risk factor for developing COPD, the disease can also be caused by breathing in dust, fumes, chemicals, and air pollution.
“Cigarette smoke or exposure to other irritants triggers inflammation and can induce cell death in the lungs and airways, which directly contributes to the development of COPD,” explains Hansbro.
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In emphysema, damage to the walls between air sacs (alveoli) in the lungs makes it more difficult to move air out of the body when exhaling. As a result, old air is trapped which leaves no room for fresh, oxygen-rich air to enter.
People with emphysema often also suffer from chronic bronchitis: an inflammation in the lining of the airways that carry air to the lungs (bronchial tubes) which causes thick mucus and a persistent cough to form.
“We investigated RIPK1 as it plays a key role in cell survival and death as well as inflammation. We found that there were far higher levels of RIPK1 in patients suffering from COPD, as well as in our COPD mouse models,” says Hansbro.
The team found that inhibiting RIPK1 activity in mice, through both knocking out the gene that produces it or introducing a compound (GSK’547) that inhibits the enzyme, had a significant protective effect against the disease.
“We saw reduced structural changes to the airways and decreased damage to the air sacs of the lungs. Our data indicates that inhibiting RIPK1 lessened both inflammation and the death of healthy lung and airway cells meaning less tissue damage overall,” adds Hansbro.
This finding represents a new promising therapeutic approach to treating COPD.