Atopic dermatitis (AD) is an inflammatory dermatosis associated with Staphylococcus aureus (S. aureus) dysbiosis. The immunological mechanisms by which S. aureus contributes to AD remain poorly characterized. We developed a mouse model of AD-like skin inflammation induced by repeated applications of different clinical strains of S. aureus, to explore the role of innate and adaptive immunity in AD. The intensity of the S. aureus-induced AD-like skin inflammation depended on the clinical strain and required the activation of the S. aureus quorum sensing. In addition, the dermatitis was hampered in inflammasome- or monocyte/macrophage-deficient animals, but not in T-cell-deficient mice, suggesting a major role of innate immunity. However, in wild type mice, a robust memory T and B cell response was detected in the weeks following S. aureus application, with an accumulation of resident memory T cells at the sites of previous dermatitis. An exaggeration of the inflammatory response was also detected after local re-exposure to S. aureus, but only in mice with an altered skin barrier. This study demonstrates the complementary role of innate and adaptive immunity in the development of an AD-like dermatitis after exposure to S. aureus.

ESDR010 - Innate and adaptive immunity to Staphylococcus aureus contribute to the development of atopic dermatitis-like skin inflammation

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