- Gene ADAM33 is heavily associated with the development of asthma
- The gene makes an enzyme which attaches to cells in the airway muscles
- But researchers say if the gene is switched off it could prevent attacks
- 300 million people worldwide suffer from the disease which can be deadly
Anna Hodgekiss for MailOnline
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Scientists have discovered a revolutionary approach which could lead to new ways of treating asthma.
Current methods of preventing attacks involve dealing with the main symptom – inflammation of the airways – which makes it difficult to breathe.
But the treatments don’t stop asthma from developing in the first place.
Researchers at the University of Southampton believe by targeting a gene called ADAM33, they can prevent the disease.
The newly-discovered genetic switch could pave the way for preventing asthma at the origin of the disease
Some 300 million people worldwide suffer from asthma – which can be deadly in severe cases.
Currently, most sufferers are treated using two inhalers.
A blue ‘reliever’ is used to relax tightened airways while a brown ‘preventer’ contains steroids which relieves inflammation in the lungs.
The researchers, writing in The Journal of Clinical Investigation, found the gene ADAM33 makes an enzyme, which is attached to cells in the airway muscles.
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In people with a variant of the gene, the enzyme detaches from the cell surface and travels around the lungs.
This then creates more muscle tissue and blood vessels around the airways which causes breathing difficulties.
But Hans Michel Haitchi, associate professor in respiratory medicine at Southampton, found switching the gene off stopped symptoms of asthma in mice.
Currently, most asthmatics are treated using two inhalers. A blue ‘reliever’ inhaler is used to relax tightened airways
He told the Daily Mail: ‘Current treatments do not treat the remodelling process in the lungs – the increase in muscle and blood vessels in the lung.
‘In future by blocking ADAM33 or preventing it from going rogue, the features of asthma – airway remodelling (more muscle and blood vessels around the airways), twitchiness and inflammation – will be reduced.’
He also said the finding dramatically changes their understanding of asthma.
Professor Haitchi added: ‘For years we have thought airway remodelling is the result of the inflammation caused by an allergic reaction, but our research tells us otherwise.’
In studies, they found a rogue ADAM33 gene caused airway remodelling, but it did not cause inflammation.
But when scientists used a house dust mite allergen – a common trigger of asthma attacks – they found it led to more muscle and blood vessels in the lungs, and inflammation.
This challenges the existing view that allergic inflammation leads to asthma in the first place.
Professor Haitchi, whose research was primarily funded by a Medical Research Council Clinician Scientist Fellowship, said: ‘Our studies have challenged the common paradigm that airway remodelling in asthma is a consequence of inflammation.
‘Instead, we have shown rogue human ADAM33 initiates airway remodelling that promotes allergic inflammation and twitchiness of the airways in the presence of allergen.
‘More importantly, we believe if you block ADAM33 from going rogue or you stop its activity if it does go rogue, asthma could be prevented.
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