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Time-saving modelling brings new insights into emphysema

Time-saving modelling brings new insights into emphysema

Prof Phil Hansbro (right) with fellow researcher Ama-Tawiah Essilfie

The race to develop urgently needed treatments for the deadly lung disorder Chronic Obstructive Pulmonary Disease (COPD), also known as emphysema, has been accelerated by new modelling developed by University of Newcastle researchers.

Prof Phil Hansbro (right) with fellow researcher Ama-Tawiah Essilfie

Prof Phil Hansbro (right) with fellow researcher Ama-Tawiah Essilfie

The race to develop urgently needed treatments for the deadly lung disorder Chronic Obstructive Pulmonary Disease (COPD), also known as emphysema, has been accelerated by new modelling developed by University of Newcastle researchers.

Where it previously took six months to conduct laboratory testing on the effects of cigarette smoke – the major cause of COPD in the Western world – the team led by Professor Phil Hansbro* has reduced the timeframe to just eight weeks.

The findings of the five-year project have been published in the prestigious international Journal of Allergy and Clinical Immunology and come as the prevalence of COPD, the fourth leading cause of chronic morbidity and death worldwide, continues to rise.

The disease is characterised by chronic airway inflammation and emphysema, which lead to breathlessness and respiratory tract infections.
“Our new modelling allows us, for the first time, to investigate the complex pathological features of the disease in a realistic timeframe,” Professor Hansbro said.

“The model we have developed helps us determine the cause of the disease and test therapies, as currently there are no treatments for emphysema.
“We can’t do this research in people because the disease takes 30 or 40 years to develop in the body, nor can we use an experimental platform that takes six months because progress is just too slow.”

Previous models looked at the responses to cigarette smoke but not the pathogenesis of the disease. Using this model, Professor Hansbro and his team also found that mast cells play a previously unidentified and damaging role in COPD.

“Mast cells are known to protect against parasites and bacteria in the body but have an inflammatory effect,” Professor Hansbro said. “We found that in the case of smokers, the mast cells respond inappropriately to airway inflammation and actually cause tissue damage.”

The lab team closely profiled the development of smoking-induced COPD over blocks of four, six, eight and 12 weeks, measuring factors such as inflammation, mucus secretion, susceptibility to infections and response to steroid treatments. The research confirmed a strong smoking-related link and has wider implications for other research modelling around the world.

* Professor Hansbro leads the University of Newcastle’s Microbiology, Asthma and Airways Research Group in the Centre for Asthma and Respiratory Disease, conducting research with Hunter Medical Research Institute’s VIVA (Viruses, Infections/Immunity, Vaccines and Asthma) Program. HMRI is a partnership between Hunter New England Health, the University of Newcastle and the community.

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