The Skin Microbiome in Atopic Dermatitis—a Potential Treatment Target?

Abstract

Staphylococcus aureus (S. aureus) frequently colonize the skin of patients with atopic dermatitis (AD). The abundance of S. aureus increases during flares, accompanied by a reduction in bacterial diversity. This flare-associated imbalance in the cutaneous microflora (dysbiosis) correlates with disease severity. However, the causality of this association has not yet been fully established, and this review aims to further explore the relation between the skin microbiome and AD along with the clinical implications hereof. Recently, it has been shown that the skin microbiome in clinically unaffected skin of AD patients differs from that of healthy individuals. In addition, mutations in the gene encoding the structural protein filaggrin (FLG) have been shown to influence the skin microbiome. Skin barrier impairments, which characterize the AD phenotype, influence the skin microbiome and increase the susceptibility to colonization with S. aureus. In turn, S. aureus can promote skin inflammation by a broad spectrum of virulence factors. Modulation of the skin microbiome by transferring beneficial skin commensals to the skin of AD patients may represent a promising strategy for the future management of AD.