Background Atopic dermatitis (AD) is associated with epidermal barrier defects, dysbiosis,
and skin injury caused by scratching. In particular, the barrier-defective epidermis in patients
with AD with loss-of-function filaggrin mutations has increased IL-1α and IL-1β levels, but the
mechanisms by which IL-1α, IL-1β, or both are induced and whether they contribute to the
aberrant skin inflammation in patients with AD is unknown. Objective We sought to
determine the mechanisms through which skin injury, dysbiosis, and increased epidermal IL …