Scientists have unearthed an unusual way of curbing the effects of asthma in a groundbreaking study that challenges our understanding of the disease.
Researchers at the University of Southampton have identified a gene, ADAM33, that appears to be linked to the life-threatening illness.
The gene creates an enzyme that attaches to cells in the airway muscles. If the enzyme loses its hold on cells’ surfaces, it tends to cause poor lung function in people with asthma.
The features of asthma include airway remodelling – the formation of extra muscle and blood vessels surrounding airways – twitchiness and inflammation.
However, when scientists were able to turn off the gene or prevent it from going rogue in human tissue samples and mice, those features were reduced.
Scientists had previously believed that allergic reactions triggered inflammation, in turn causing the airways to remodel. But Southampton’s Professor Hans Michel Haitchi said the research tells us otherwise.
The team conducted several studies which suggested that airway remodelling was triggered by the gene. When mice that had the gene removed were introduced to a common allergen, airway remodelling and inflammation were reduced by 50% and 35% respectively.
Haitchi added: “We believe that if you block ADAM33 from going rogue or you stop its activity if it does go rogue, asthma could be prevented. 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 UK has one of the highest rates of asthma in Europe. Of the 5 million people who suffer from the disease, 1.1 million are children aged between 1 and 11. It costs the NHS around £1bn a year to treat and care for people living with the illness.
Haitchi’s study was published in the The Journal of Clinical Investigation (JCI) Insight.