Millions of asthma sufferers are able to regulate their symptoms with inhalers. However, about 5 percent of patients do not respond to any treatment.
Scientists claim to have found a breakthrough; the root cause of asthma, which could pave the way for a new treatment within five years.
Scientists have found a protein within the airways which they believe triggers all asthma attacks
Scientists have found a protein within the airways which they believe triggers all asthma attacks. A drug already exists they think could deactivate the protein, raising hopes for a treatment for an asthma patient.
The team was led by Cardiff University, has shown that the drug works in mice and human tissue samples in the laboratory. They have designed the first clinical trials that could possibly start within two years.
Professor Daniela Riccardi, a lead investigator said: ‘Our findings are incredibly exciting.’
Professor Riccardi said the discovery came by chance when, formerly a bones specialist, switched from the study of osteoporosis to the study of the lungs five years ago. That is when she realized a protein that triggers the growth of calcium within bones also plays a role in the airways.
In further tests, asthmatics had far higher levels of the protein – called a ‘calcium-sensing receptor’ or CaSR than healthy people. When an asthmatic breathes in triggers, i.e. dust, smoke, or pollen, the CaSR molecules cause the rapid increase of calcium within the cells of the lung tissue. When the added calcium makes the cells contract and the airways spasm, it triggers an asthma attack.
Professor Riccardi said: ‘For the first time we have found a link between airways inflammation, which can be caused by environmental triggers – such as allergens, cigarette smoke, and car fumes – and airways twitchiness in allergic asthma.
‘It makes the cells much more sensitive to the asthma triggers – which then make an attack much more likely.’
There is a drug that already exists, that can disable the CaSR protein, meaning it could be available to patients as soon as clinical trials are complete.
The medication is called a calcilytic, was developed 15 years ago to knock out the same protein in osteoporosis. The drug was shown to be safe, but it was not useful for osteoporosis patients.
Early tests in mice and human tissue showed promising results as an asthma treatment.
Scientists from King’s College London and the Mayo Clinic in the US, who were also on the team, hope to use the drug in a nebulizer, where it is turned into a mist and breathed straight into the lungs.
When an asthmatic breathes in triggers such as dust, smoke, or pollen, the newly-identified protein causes the rapid increase of calcium within the cells of the lung tissue. This makes the cells contract and the ing the airways spasm, triggering an asthma attack
A few courses of treatment would be enough to stop asthma attacks from recurring, they hope.
The suspect it might also have a role in tackling chronic obstructive pulmonary disease – COPD – and chronic bronchitis, for which there is currently no effective treatment.
Prof Riccardi said: ‘If we can prove that calcilytics are safe when administered directly to the lung in people, then in five years we could be in a position to treat patients and potentially stop asthma from happening in the first place.’
Dr. Samantha Walker, director of research at Asthma UK, who helped fund the research, added: ‘This hugely exciting discovery enables us, for the first time, to tackle the underlying causes of asthma symptoms.
‘Five percent of people with asthma don’t respond to current treatments so research breakthroughs could be life-changing for hundreds of thousands of people.
‘If this research proves successful we may be just a few years away from a new treatment for asthma, and we urgently need further investment to take it further through clinical trials.
‘Asthma research is chronically underfunded; there have only been a handful of new treatments developed in the last 50 years so the importance of investment in research like this is absolutely essential.’
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