010 Skin dysbiosis promotes autoimmune inflammation via neutrophil activation and the IL-23/IL-17 axis

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease, but its etiology is not completely understood. Recently, the microbiotas in the nasal cavity and gut have been shown to be involved in the development of SLE, but the influence of skin microbiota is still unclear. Here, we demonstrated that NfkbizΔK5 mice treated with Staphylococcus aureus develop SLE-associated autoantibodies and glomerulonephritis with IgG deposition. Epicutaneous S. aureus application significantly increases staphylococcal colonization in the skin of NfkbizΔK5 mice with reduced expression of antimicrobial peptides, which promotes caspase-mediated keratinocyte apoptosis and neutrophil activation, inducing the IL-23/IL-17 immune response by activating dendritic cells and T cells.