Scientists at Imperial College London in the UK have discovered over 30 new genes that predispose individuals to both asthma and allergies such as eczema and hay fever.
The study, published in Nature, took 10 years to complete and involved researchers based in the UK, US, Canada and Sweden. Their findings could be used to develop new treatments for these diseases, as well as help calculate which patients will respond best to currently-used treatments.
“The genes we identified represent new potential drug targets for allergic diseases as well as biomarkers that may predict which patients will respond to existing expensive therapies,” says Prof. Miriam Moffatt, one of the study’s authors.
Asthma is a widespread condition, affecting 8% of adults in the US – around 18.7 million people – according to the Centers for Disease Control and Prevention (CDC).
For the study, the researchers decided to investigate epigenetic changes – those influencing the activity of genes, rather than changes affecting the genetic code itself. With this approach, the team could pinpoint genes regulating an antibody associated with the triggering of allergic reactions.
Prof. William Cookson, another of the study’s authors, explains that their pioneering epigenetic approach allowed them to gain insights that traditional genetics could not provide:
“It isn’t just the genetic code that can influence disease and DNA sequencing can only take you so far. Our study shows that modifications on top of the DNA that control how genes are read may be even more important.”
The antibody in question is called immunoglobin E (IgE). Although its involvement in triggering allergic responses was already known, researchers did not know which genes were responsible for regulating its activities.
“Asthma, atopic dermatitis (eczema) and hay fever are IgE-related diseases that are increasing in prevalence and are a major source of disability,” write the authors. “Therapies directed against IgE can alleviate hay fever and allergic asthma.”
White blood cells from a total of 355 participants with asthma were analyzed. The researchers assessed whether levels of methylation – a process in which genes are rendered inactive through the attachment of methyl molecules to their DNA – were associated with the level of IgE in the blood.
Strong associations were seen between IgE and low levels of methylation in 34 genes. These genes are far more active in people with asthma, leading to the production of greater quantities of IgE that help trigger the symptoms of the disease.
These findings were also checked against additional volunteers from Wales with either high or low levels of IgE in their bloodstreams and another 160 participants from Québec, Canada, with doctor-diagnosed asthma.
A number of the newly-identified genes had been demonstrated to encode proteins produced by a specific type of white blood cell – eosinophils – known to promote inflammation in the airways of people with asthma. The study authors state that these genes activate eosinophils, leading to asthma symptoms.
The discovery of a new way in which eosinophils are activated means that doctors may be able to identify which asthma patients will respond to therapies that neutralize these white blood cells. At present, these therapies are expensive and only work for some people with the condition.
Funding for the study came from the Wellcome Trust, the Freemasons’ Grand Charity and the Québec Government.
Recently, Medical News Today reported on a mouse study finding that the development of asthma could be prevented with low concentrations of a psychedelic drug.