Dysbiosis and Staphyloccus aureus Colonization Drives Inflammation in Atopic Dermatitis

Staphyloccus aureusskin colonization is universal in atopic dermatitis and common in cancer patients treated with epidermal growth factor receptor inhibitors. However, the causal relationship of dysbiosis and eczema has yet to be clarified. Herein, we demonstrate thatAdam17fl/flSox9-Cremice, generated to modelADAM17-deficiency in human, developed eczematous dermatitis with naturally occurring dysbiosis, similar to that observed in atopic dermatitis.Corynebacterium mastitidis,S. aureus, andCorynebacterium bovissequentially emerged during the onset of eczematous dermatitis, and antibiotics specific for these bacterial species almost completely reversed dysbiosis and eliminated skin inflammation. WhereasS. aureusprominently drove eczema formation,C. bovisinduced robust T helper 2 cell responses. Langerhans cells were required for eliciting immune responses againstS. aureusinoculation. These results characterize differential contributions of dysbiotic flora during eczema formation, and highlight the microbiota-host immunity axis as a possible target for future therapeutics in eczematous dermatitis.