Eczema is one of the most common skin conditions, affecting roughly one in 10 adults. Now, new research has suggested that a deficiency in the skin's outer barrier is key to triggering the debilitating problem, leaving scientists one step closer to discovering exactly what it is that triggers eczema and what they can do to prevent it.
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The Newcastle University research team created a human model system in their laboratory in order to mimic the skin observed in patients with atopic eczema the most common type. They then used molecular techniques to reduce the levels of filaggrin, the protein which has previously been strongly linked to eczema, within the upper layer of skin (epidermis) of the model.
A number of regulatory mechanisms, such as stress responses, were affected by the changes. Nick Reynolds, Professor of Dermatology at Newcastle University and who works within the Newcastle Hospitals NHS Foundation Trust is the lead investigator of the study. He said:
"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. This research reinforces the importance of filaggrin deficiency leading to problems with the barrier function in the skin and predisposing someone to eczema."
Other mechanisms affected by altered filaggrin levels included inflammatory signalling, cell structure and barrier function all of which are known to be active in the skin of patients with eczema. Nina Goad of the British Association of Dermatologists said:
"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. 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 paper was published in the Journal of Allergy and Clinical Immunology.
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