Atopic dermatitis (AD) is a chronic, common inflammatory skin disease affecting 15-20% of children and 1-3% of adults worldwide.

Loss of bacterial diversity from excess abundance of Staphylococcus aureus is associated with increased disease severity, nevertheless, how dysbiosis of the skin microbiome may influence atopic dermatitis pathophysiology is unknown. In this recent study, Williams et al. show that protease and phenol-soluble modulin-α (PSMα ) secreted by S. aureus cause epidermal proteolysis and skin barrier damage in human keratinocytes, skin and mice, thus promoting inflammation.

Human keratinocyte cytokine protein expression of IL-6, TNF-α, IL-1α treated with supernatant from an overnight culture of S. aureus wild-type (WT) or SA phenol-soluble modulin alpha (∆psmα) and SA phenol-soluble modulin beta (∆psmβ) knock out strain supernatants for 24h.

Coagulase-negative staphylococci (CoNS), including S. epidermidis and S. hominis that are normally present on human skin were shown to secrete autoinducing peptides (AIP) that inhibit accessory gene regulator quorum sensing in S. aureus, thus reducing PSMα expression. These autoinducers also reduced S. aureus-induced dermatitis in mice.

Skin microbiome analyses of individuals with atopic dermatitis suggested that the ratio of CoNS to S. aureus has a role in atopic dermatitis pathogenesis

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Source : Quorum sensing between bacterial species on the skin protects against epidermal injury in atopic dermatitis


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