Genes responsible for Asthma uncovered

Epigenetic factors behind asthma and other allergic diseases have been identified by a group at Imperial College in research that could lead to better targeted and more effective treatments. Their paper, published in Nature, identifies 34 genes related to inflammation, inhibited in healthy people, but overexpressed in those with allergies.

Epigenetics has been a bit of a buzzword in biology in the past few years, as it seems to provide an explanation for many complex aspects of life that cannot be explained by a naïve interpretation of how our genes work.

Simply having a gene doesn’t mean it will be expressed. Environmental factors can turn them on or off by adding methyl groups at specific points on the DNA, which prevent it being read and forming proteins. Levels of methylation have been linked to ageing and the growth of cancers, and could even provide some explanation for the beneficial effects of exercise, and the lifelong negative effects of childhood traumas.

The researchers analysed the blood of people with asthma and measured the level of methylation of genes that regulate the production of IgE (Immunoglobulin E), an antigen that causes inflammation. They found 36 locations on 34 genes that had very low levels of methylation in those with asthma. There was a strong correlation between the activity of these genes and the levels of IgE in the patient’s blood. These findings were backed up by similar results obtained by a group in Canada.

Some of the genes identified encode proteins produced by eosinophils, a type of white blood cell known to cause inflammation in the lungs. Drugs to reduce the activity of eosinophils are sometimes given to asthma sufferers, but this new research could allow genetic testing to identify people who could benefit from them. It also offers potential targets for new classes of drugs to treat patients whose asthma does not respond well to current treatments.

5 million people in the UK are currently receiving treatment for asthma, which is caused when the airways of the lungs become inflamed and narrowed, restricting the passage of air. It is closely related to eczema and hay fever, the so-called ‘atopic triad’, which are also caused by high IgE levels.

The research was led by Miriam Moffatt and William Cookson from the National Heart and Lung Institute. Professor Cookson said: “Our pioneering approach, using epigenetics, allowed us to obtain insights that we weren’t able to get from traditional genetics. 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.”