Abstract
OTULIN is a deubiquitinase that specifically cleaves linear ubiquitin chains. We demonstrate that ablation of OTULIN selectively in keratinocytes, results in the appearance of inflammatory skin lesions that develop into verrucous carcinomas. Genetic ablation of TNFR1, knockin expression of kinase-inactive RIPK1 or keratinocyte-specific deletion of FADD and MLKL completely rescues mice with OTULIN deficiency from dermatitis and tumorigenesis, identifying keratinocyte cell death as the driving force for inflammation.
Highlights
The skin commensal Staphylococcus epidermidis induces inflammatory mediators in keratinocytes: Implications for atopic dermatitis D Ochlich, F Rademacher, KA Drerup, A Weingartner, R Glaser and J Harder Dermatology, University Hospital Schleswig-Holstein, Kiel, Germany The chronic inflammatory skin disease atopic dermatitis (AD) is characterized by a dysbiosis of the microbiota
S. epidermidis strains derived from lesional AD skin induced a higher thymic stromal lymphopoietin (TSLP) expression than strains derived from healthy skin
S. epidermidis strains derived from healthy skin and strains derived from AD skin activated the inflammation-associated transcription factor NF-kappaB
Summary
The skin commensal Staphylococcus epidermidis induces inflammatory mediators in keratinocytes: Implications for atopic dermatitis D Ochlich, F Rademacher, KA Drerup, A Weingartner, R Glaser and J Harder Dermatology, University Hospital Schleswig-Holstein, Kiel, Germany The chronic inflammatory skin disease atopic dermatitis (AD) is characterized by a dysbiosis of the microbiota. A microarray analysis reported expression of IL-2Rg by keratinocytes in reconstructed human epidermis (RHE) exposed to IL-4, IL-13 and IL-25. To evaluate this hypothesis we stimulated cultured human keratinocytes and 3D skin models with different S. epidermidis isolates derived either from healthy skin or from lesional skin of AD patients.
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