Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a dysregulated immune response associated with barrier dysfunction and dysbiosis of the skin microbiota characterized by Staphylococcus aureus colonization in lesional skin. The aim of our study was to compare non-lesional and lesional AD skin transcriptional profile depending on staphylococcal colonization. Skin biopsies were analyzed by RT-qPCR in moderate and severe adults AD patients. Staphylococcus epidermidis was detected in all lesional skin, in greater abundance than in non-lesional skin, while S. aureus colonization was found in approximatively 50% of AD patients. Our results suggest a greater decrease of gene expression involved in skin differentiation (FLG, CLDN-1, LOR, GATA3) in lesional skin colonized by S. aureus. Interestingly, up-regulation of chemokines and cytokines involved in AD pathogenesis (including IL13, TSLP, CCL17, and CCL18) in lesional skin was not impacted by S. aureus colonization, excepted for CCL22 expression which was weaker in the presence of S. aureus colonization. These findings suggest a role of S. aureus in barrier dysfunction and inflammatory response in AD lesional skin.

ESDR032 - Impact of Staphylococcus aureus colonisation on barrier function and cytokine profile in atopic dermatitis skin.

50th Annual Meeting of the European Society for Dermatological Research. VIRTUAL MEETING