Scientists have discovered a genetic switch that could pave the way for preventing asthma at the origin of the condition.
The research carried out at the University of Southampton, published in The Journal of Clinical Investigation (JCI) Insight, analysed the impact of the gene ADAM33, which is associated with the development of asthma.
ADAM33 makes an enzyme attached to cells in the airway muscles.
When the enzyme loses its anchor to the cell surface, it is prone to going rogue around the lung causing poorer lung function in people who have asthma.
The studies in human tissue samples and mice, led by Hans Michel Haitchi, associate professor in respiratory medicine, suggests that if you switch off ADAM33 or prevent it from going rogue, the features of asthma - airway remodelling (more muscle and blood vessels around the airways), twitchiness and inflammation - will be reduced.
Prof Haitchi said: "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."
The first study showed rogue human ADAM33 caused airway remodelling resulting in more muscle and blood vessels around the airways of developing lungs, but it did not cause inflammation.
When a common house dust mite allergen was introduced airway remodelling and allergic airway inflammation were more significantly enhanced.
In another study, remodelling of the airway was shown in mice that had ADAM33 switched on in utero.
The gene was then switched off and the airway remodelling reversed.
They also studied the impact of house the dust mite allergen on asthma features in mice that had the ADAM33 gene removed.
Airway remodelling and twitchiness as well as airway inflammation rates were significantly reduced by 50 per cent and 35 per cent respectively in mice that did not have the rogue gene.
Prof Haitchi, whose research was primarily funded by a Medical Research Council Clinician Scientist Fellowship, said: "We have shown that rogue human ADAM33 initiates airway remodelling that promotes allergic inflammation and twitchiness of the airways in the presence of allergen.
"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.
"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."
