Mouse gene aids allergy research

Eczema can cause the skin to become very red and itchy

A genetic defect discovered in mice could help scientists find out what is responsible for the large increase in allergic diseases seen in recent years.

Researchers in Dundee, Ireland and Japan said the defect in mice leads to allergic inflammation, comparable to that seen in human eczema.

They believe it confirms the importance of the filaggrin gene, which helps skin produce a protective barrier.

The barrier stops allergens which lead to eczema and asthma entering the body.

It also helps keep out the foreign bodies which can trigger hay fever and other allergies and prevents water loss from the skin.

About one in five children in Britain and other westernised nations suffer from eczema, according to the scientists.

These mice also represent a key to unlock new and improved therapies for eczema, asthma and allergies Prof Irwin McLean

Eczema can range from a slightly irritating patch of sore skin to more extreme cases where extensive areas may become inflamed and unbearably itchy.

Children with the condition are more likely to subsequently develop other allergic conditions, in particular asthma, but also hay fever and others.

Previous work on the subject suggested that up to a half of cases of severe eczema in children were associated with genetic mutations in the filaggrin gene.

The filaggrin gene defects are carried by more than 10% of the UK population.

Professor Irwin McLean, from Dundee University, said it was "amazing" to find a filaggrin gene defect in mice which was essentially identical to human mutations.

"The prevalence of eczema, asthma and allergies has increased considerably in recent decades and this is most likely due to unknown environmental factors," he said.

"The filaggrin-deficient mice will allow us to identify key substances in the environment responsible for the huge increase in allergic disease.

"These mice also represent a key to unlock new and improved therapies for eczema, asthma and allergies by targeting or supplementing the defective filaggrin gene.

"Drugs or other treatments aimed at the filaggrin gene are still some years away but this work is a major step in the right direction and should give hope to those with these distressing conditions."