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Centenary Institute - Medical Research
Centenary Institute - Medical Research

Inflammation in the spotlight

The Centenary Institute has held its inaugural ‘Inflammation Symposium’ on 13 and 14 July, highlighting the latest in medical research across the field of inflammation and disease.

Bringing together Centenary researchers, as well as world-leading inflammation researchers from across Australia and overseas, the aim was to feature the strength of Centenary’s inflammation research, to promote discussion and to extend collaboration opportunities to maximise research outcomes.

Professor Phil Hansbro (pictured), Director of the Centenary UTS Centre for Inflammation and symposium convener, was pleased at how successful and informative the two-day symposium was.

“We were delighted to have presentations from experts from high profile inflammation centres located within the University of Queensland; the Hudson and Garvan Institutes of Medical Research and the University of Manchester (UK).”

“The symposium provided an ideal platform to define capabilities and to explore ways to potentially extend research activity and collaborations between institutions. Enabling collaborations can benefit investigator studies and can also aid in developing new funding opportunities,” said Professor Hansbro.

Presentations at the symposium included current studies on lung and mucosal immunity, liver inflammation, the aged vasculature and the role of the gut-lung axis in chronic obstructive pulmonary disease (COPD).

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Cell death discovery could lead to new treatment for COPD

Research shows that inhibiting necroptosis, a form of cell death, could be a novel therapeutic approach for treating chronic obstructive pulmonary disease (COPD), an inflammatory lung condition, also known as emphysema, that makes it difficult to breathe.

Published in the prestigious ‘American Journal of Respiratory and Critical Care Medicine’, the study by a team of Australian and Belgian researchers, revealed elevated levels of necroptosis in patients with COPD.

By inhibiting necroptosis activity, both in the lung tissue of COPD patients as well as in specialised COPD mouse models, the researchers found a significant reduction in chronic airway inflammation as well as damage to the lung.

Professor Phil Hansbro (pictured), Director of the Centenary UTS Centre for Inflammation who led the research team, said that necroptosis was a form of cell death known to drive tissue inflammation and destruction.

“Necroptosis, apoptosis and necrosis are all forms of cell death but they operate in distinctly different ways. Significantly, in necroptosis, a cell bursts, dispersing its contents into nearby tissues resulting in an immune and inflammation response.”

“Our research suggests that inhibiting necroptosis and preventing this inflammation response may be a new therapeutic approach to treating COPD,” said Professor Hansbro.

Joint first author on the study, Dr Zhe Lu, a researcher at the University of Newcastle, said that their study was the first of its type to be able to distinguish between the roles of necroptosis and apoptosis in COPD.

“Necroptosis is generally pro-inflammatory. Apoptosis, however, tends to be non-inflammatory as it’s a more ordered form of cell death–a cell self-degrades as opposed to bursting and there’s no leakage of cell contents. This may explain why, in our study, it’s the inhibition of necroptosis and not apoptosis that reduces lung damage and COPD associated inflammation,” said Dr Lu.

A debilitating respiratory condition and a leading cause of death worldwide, there are currently no treatments that halt or reverse the progression of COPD.

“Our research suggests that it is the type of cell death associated with COPD that is important and that the development of new drugs that can interfere or intervene in the necroptosis process could be a new targeted therapy for this common lung disease,” said Professor Hansbro.

The study was led by researchers from the Centenary Institute, University of Technology Sydney, University of Newcastle, Ghent University, Belgium and Ghent University Hospital, Belgium.

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Publication: Necroptosis Signalling Promotes Inflammation, Airway Remodelling and Emphysema in COPD. American Journal of Respiratory and Critical Care Medicine.

Gut microbiome link to deadly lung disease

Research led by the Centenary Institute, the University of Technology Sydney and the University of Queensland has shown for the first time a link between chronic obstructive pulmonary disease (COPD), an often fatal lung condition, and the gut microbiome.

The findings, published in the high impact science journal ‘Nature Communications’, suggest that the gut may be helpful in diagnosing COPD and may also be a potential source of new therapeutic targets to help treat the chronic respiratory disorder.

“It’s already known that the lung microbiome is a contributing factor in COPD,” said Professor Phil Hansbro (pictured), senior author of the study and Director of the Centenary UTS Centre for Inflammation.

“We wanted to see if the gut environment was also somehow involved–to determine whether the gut could act as a reliable indicator of COPD or if it was connected in some way to the development of the disease.”

In the study, the researchers compared the microbiome and metabolite profiles of stool samples from COPD patients with healthy individuals. Revealed were significant differences between the two groups.

COPD patients exhibited increased levels of the bacteria Streptococcus and Lachnospiraceae in their stool samples. Also identified in individuals with COPD was a unique metabolite signature–formed by the chemical by-products of the metabolic process.

“Our research indicates that the gut of COPD patients is notably different from healthy individuals,” said first author on the paper Dr Kate Bowerman, University of Queensland.

“This suggests that stool sampling and analysis could be used to non-invasively diagnose and monitor for COPD,” she said.

The study’s researchers believe that the altered gut microbiome found in COPD patients could also support the gut as a potential target for new treatments.

“The ‘gut-lung axis’ describes the common immune system of the lung and gastrointestinal tract. This means that activity in the gut can impact activity in the lung. Our COPD findings suggest that the gut microbiome should now also be considered when looking for new therapeutic targets to help treat lung disease,” said Professor Hansbro.

COPD, a life threatening inflammatory disorder of the lungs, is the third most common cause of death globally. More than 3 million lives are lost every year to COPD.

Researchers involved in the study were affiliated with The University of Queensland, Hunter Medical Research Institute, University of Newcastle, The Prince Charles Hospital, Centenary Institute and University of Technology Sydney.

Publication: Disease-associated gut microbiome and metabolome changes in patients with chronic obstructive pulmonary disease.

Read more about our COPD related medical research here.

New treatment hope for asthma and COPD

An international study led by the University of Glasgow, including collaborators from the Centenary Institute, has identified a new class of drugs that could pave the way to a new treatment for asthma and chronic obstructive pulmonary disease (COPD).

The breakthrough findings, published in the journal ‘Science Translational Medicine’, found that the drugs were able to reverse the symptoms of asthma in animal models.

Researchers also found that the same drugs, when applied to lung samples obtained from human donors, showed effects similar to those seen in the animal models.

Scientists believe that these combined findings offer new hope that these drugs could provide new medicines for human inflammatory lung disease.

The new approach is centred on the activation of a protein that, up until now has been known to respond to good fats contained in our diet. The protein, called free fatty acid receptor 4 (FFA4), is found in the gut and pancreas where it is activated by good dietary fats including the fish oil omega 3. Once activated FFA4 is known to help control levels of glucose in the blood.

Surprisingly the research team found FFA4 to be present in the human lung.

By designing a new class of drugs that activate FFA4 in the lung, the researchers found that the muscle that surrounds the airways relaxes allowing more air to enter the lung. They also found that activators of FFA4 reduced inflammation caused by exposure of mice to pollution, cigarette smoke and allergens like house dust mite that cause asthma.

In this way the researchers have established that activating FFA4 can reverse the key hallmarks of inflammatory lung disease heralding the prospect of new drugs for the treatment of lung disease.

“The study was a truly collaborative effort with some of the experimental work done here in Australia, utilising our world-class facilities, said Professor Phil Hansbro, co-author on the published study and Director of the Centenary UTS Centre for Inflammation.

“I’m optimistic that this breakthrough could lead to life-changing treatments for sufferers of asthma and COPD, both of which can be devastating and deadly diseases,” he said.

Photo (L to R): Publication co-authors from the Centenary Institute, Dr Richard Kim, Professor Phil Hansbro, Dr Chantal Donovan.

The full media release can be found here.

The research publication can be found here.