Researchers from Newcastle University, U.K., in collaboration with scientists at Stiefel, a GSK company, have identified how the skin barrier protein filaggrin impacts the development of eczema through its interactions with other proteins and pathways in the skin.
In a press release from the university, lead author Professor Nick Reynolds, MD, 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.”
Dr. Reynolds is Professor of Dermatology at the university.
Investigators created a human model system in which the epidermis was modified to become filaggrin-deficient, directly mimicking the situation observed in the skin of patients with atopic eczema.
Once they had this model, the researchers were able to identify proteins and signalling pathways directly downstream of filaggrin, as well as a number of key regulatory mechanisms. These included regulators of inflammatory signalling, cell structure, barrier function and stress response.
The identified molecular pathways were found to map to networks observed in the skin of people with active eczema.
Understanding these connections provides eczema researchers with new understanding of the mechanisms behind the condition and suggests potential new targets for therapy, according to the release.
Nina Goad, Head of Communications for the British Association of Dermatologists, said in the release: “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.”