Scientists have come a step closer to developing a cure for eczema after discovering how a deficiency in the skin’s natural barrier can trigger the painful condition.
Eczema, which causes the skin to become dry, red and itchy, affects one in five children and one in 12 adults in the UK, according to the National Eczema Society.
Flare-ups can be treated with creams and steroids, but there is currently no cure for the disorder.
Several years ago, researchers at the University of Dundee found the lack of a skin protein called filaggrin caused an inherited skin condition related to eczema, called ichthyosis vulgaris.
Genetic mutations can cause filaggrin, which plays an important role in protecting the skin from irritants, to stop working correctly.
Now scientists have built on this knowledge to better understand why some people develop atopic eczema, dry skin which often appears on the hands, insides of the elbows, backs of the knees and the face and scalp in children.
“We have shown for the first time that loss of the filaggrin protein alone is sufficient to alter key proteins and pathways involved in triggering eczema,” said Nick Reynolds, a dermatology professor at Newcastle University.
“This research reinforces the importance of filaggrin deficiency leading to problems with the barrier function in the skin and predisposing someone to eczema.“
Professor Reynolds and his team said their findings, published in the Journal of Allergy and Clinical Immunology, could help drug researchers to pinpoint the causes of eczema and develop a cure for the condition, rather than treating the symptoms.
Their research involved creating a model of human skin in a lab, which they modified using molecular techniques to create a filaggrin deficiency in the skin’s barrier.
They then studied a number of other biological mechanisms affected by the protein, which control cell structure and stress responses and can trigger skin inflammation.
The researchers compared their findings to the way skin affected by eczema behaves, and noticed significant similarities.
“This latest research from Newcastle is crucial as it expands on our knowledge of how filaggrin impacts on other proteins and pathways in the skin, which in turn trigger the disease,” said Nina Goad of the British Association of Dermatologists.
“This type of research allows scientists to develop treatments that target the actual root cause of the disease, rather than just managing its symptoms. Given the level of suffering eczema causes, this is a pivotal piece of research.”
The research was conducted in collaboration with scientists at pharmaceutical company Stiefel.
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