Atopic dermatitis (AD), or eczema, is an inflammatory skin disease that affects 20 percent of children and about 5 percent of adults. Staphylococcus aureus colonization during AD contributes to skin inflammation, but the underlying mechanisms are unclear. We demonstrate that S. aureus-driven skin inflammation is mediated by bacterial toxin PMSα and the protein produced in our skin called IL-36. We found that normal mice develop scaly and inflamed skin after S. aureus colonization, but the genetically engineered mice lacking IL-36 activity had almost no skin inflammation. Therefore, IL-36 could be a potential biologic treatment target for AD. This research was done at Dr. Lloyd Miller’s lab in the Department of Dermatology.