Abstract
Atopic dermatitis (AD) is a widespread chronic inflammation of the skin with a diverse and complex pathogenesis. AD is characterized by a dysregulation of barrier molecules such as keratins and filaggrin (FLG) including FLG mutations. In addition, a dysbiosis of the cutaneous microbiota is associated with AD. However, it is still not completely understood whether the dysbiosis of the cutaneous microbiota is a cause or a consequence of the destroyed integrity of the skin barrier in AD. Functional approaches to address this question are rare.
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