An Inflamed and Infected Reconstructed Human Epidermis to Study Atopic Dermatitis and Skin Care Ingredients
Autor: | Sébastien Cadau, Manon Gault, Nicolas Berthelemy, Chiung-Yueh Hsu, Louis Danoux, Nicolas Pelletier, Dominique Goudounèche, Carole Pons, Corinne Leprince, Valérie André-Frei, Michel Simon, Sabine Pain |
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Rok vydání: | 2022 |
Předmět: |
Staphylococcus aureus
Organic Chemistry General Medicine Staphylococcal Infections Skin Care Catalysis Dermatitis Atopic Computer Science Applications Inorganic Chemistry atopic dermatitis inflammation microbiota epidermal barrier lamellar body tissue engineering Humans Cytokines Epidermis Physical and Theoretical Chemistry Molecular Biology Spectroscopy Skin |
Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 21; Pages: 12880 |
ISSN: | 1422-0067 |
DOI: | 10.3390/ijms232112880 |
Popis: | Atopic dermatitis (AD), the most common inflammatory skin disorder, is a multifactorial disease characterized by a genetic predisposition, epidermal barrier disruption, a strong T helper (Th) type 2 immune reaction to environmental antigens and an altered cutaneous microbiome. Microbial dysbiosis characterized by the prevalence of Staphylococcus aureus (S. aureus) has been shown to exacerbate AD. In recent years, in vitro models of AD have been developed, but none of them reproduce all of the pathophysiological features. To better mimic AD, we developed reconstructed human epidermis (RHE) exposed to a Th2 pro-inflammatory cytokine cocktail and S. aureus. This model well reproduced some of the vicious loops involved in AD, with alterations at the physical, microbial and immune levels. Our results strongly suggest that S. aureus acquired a higher virulence potential when the epidermis was challenged with inflammatory cytokines, thus later contributing to the chronic inflammatory status. Furthermore, a topical application of a Castanea sativa extract was shown to prevent the apparition of the AD-like phenotype. It increased filaggrin, claudin-1 and loricrin expressions and controlled S. aureus by impairing its biofilm formation, enzymatic activities and inflammatory potential. |
Databáze: | OpenAIRE |
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