In two publications in the Journal of Clinical Immunology and Allergy, researchers from the Experimental Dermatology Laboratory, themes Inflammatory diseases and Infectious diseases and global health have revealed novel insights into the functional role of the filaggrin protein in the skin. These studies significantly contribute to the current knowledge on the pathogenesis of atopic dermatitis, or eczema, as loss-of-function mutations in the Filaggrin gene are the major risk factor for this very common chronic inflammatory skin disease.
The paper first authored by Hanna Niehues, PhD candidate (photo up), concludes that a total FLG deficiency does not have a major impact on the skin barrier function. The current dogma stated that the loss of FLG protein leads to barrier defects and thus a higher exposure by potential allergens that triggers inflammation. The paper by Niehues et al. will therefore change the current view and poses a challenge to find an alternative explanation for the link between the loss of FLG and atopic dermatitis.
Patrick Zeeuwen together with colleagues from the Dermatology department and collaborators from the NIZO food research and the Centre for Molecular and Biomolecular Informatics (CMBI) found that specific commensal bacteria that utilize FLG breakdown products as their source of nutrients are depleted in FLG deficient individuals. Studies on the interaction of these commensal bacteria with keratinocytes suggest that absence due to the FLG deficiency may alter host defense mechanisms and thereby contribute the atopic dermatitis disease pathogenesis.
- Epidermal equivalents of filaggrin null keratinocytes do not show impaired skin barrier function. J Allergy Clin Immunol.
- Gram-positive anaerobe cocci (GPAC) are underrepresented in the microbiome of filaggrin-deficient human skin. J Allergy Clin Immunol.
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