Deficiency of a protein that acts as a skin barrier is responsible for triggering eczema -- an itchy inflammation of the skin, scientists said. Atopic eczema is a common skin condition and often found in children in the first year of their life and persists into adulthood with severe itching that has profound effects on well-being and may lead to sleep disturbance.
The findings showed that the lack of protein filaggrin impacts other proteins and pathways in the skin, which in turn drive the development of eczema.
"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, Professor Dermatology at Newcastle University in England.
"This research reinforces the importance of filaggrin deficiency leading to problems with the barrier function in the skin and predisposing someone to eczema."
For the study, published in the Journal of Allergy and Clinical Immunology (JACI), the team developed a human model system. Using molecular techniques, the upper layer of the skin (epidermis) was modified, to become filaggrin-deficient, as observed in the skin of patients with atopic eczema.
The model enabled the researchers to discover proteins and signalling pathways directly down-stream of filaggrin, and most importantly, identified a number of key regulatory mechanisms.
These included regulators of inflammatory signalling, cell structure, barrier function and stress response. This mapping provides new understanding of the mechanisms involved and suggests targets for future drug development, which could treat the underlying cause rather than treating the symptoms, the researchers said.