Asthma cure on the horizon, according to University of Southampton study

Asthma could be stopped by switching off the gene which causes it, British scientists found

Megan White
Thursday 21 July 2016 14:24
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Scientists have discovered a genetic switch which could prevent asthma at its origin
Scientists have discovered a genetic switch which could prevent asthma at its origin

Researchers have discovered a novel way of preventing asthma at the origin of the disease, a finding that could challenge the current understanding of the condition.

The Southampton university team, led by associate professor in respiratory medicine Hans Michael Haitchi, analysed the impact of the gene ADAM33, which is associated with the development of asthma.

An enzyme produced by the gene attaches to cells in airway muscles, which can run rogue and cause poor lung function in those affected by the condition.

The studies in human tissue samples and mice suggest that if you switch off ADAM33 or prevent it from going rogue, the symptoms of asthma – more muscle and blood vessels around the airways, twitchiness and inflammation – will be reduced.

Professor Haitchi said: “This finding radically alters our understanding of the field, to say the least.

For years we have thought that airway remodelling is the result of the inflammation caused by an allergic reaction, but our research tells us otherwise.

More importantly, we believe that if you block ADAM33 from going rogue or you stop its activity if it does go rogue, asthma could be prevented.

The first study showed that rogue human ADAM33 causes airway remodelling, resulting in more muscle and blood vessels around the airways of developing lungs, but not inflammation. But when a house dust mite allergen was introduced – a very common human allergen – both airway remodelling and allergic airway inflammation were more significantly enhanced.

Scientists also studied the impact of house dust mite allergen on asthma features in mice that had the ADAM33 gene removed. Airway remodelling, twitchiness and airway inflammation rates were reduced by 50 per cent in mice that did not have the rogue gene.

These findings identify ADAM33 as a novel target for disease modifying therapy in asthma.

Professor Haitchi added: Our studies have challenged the common paradigm that airway remodelling in asthma is a consequence of inflammation. Instead, we have shown that rogue human ADAM33 initiates airway remodelling that promotes allergic inflammation and twitchiness of the airways in the presence of allergen.”

“ADAM33 initiated airway remodelling reduces the ability of the lungs to function normally, which is not prevented by current anti-inflammatory steroid therapy. Therefore, stopping this ADAM33-induced process would prevent a harmful effect that promotes the development of allergic asthma for many of the 5.4 million people in the UK with the condition.

The research was published in the Journal of Clinical Investigation.

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