Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. The skin of patients with AD presents as a disbalance of the microbiome with a strong colonization by Staphylococcus aureus, which positively correlates with the severity of the disease. In addition, S. aureus isolated from patients with AD was reported to be more likely to produce superantigens. However, the effect of colonized S. aureus on the skin immune system has not been fully elucidated. 
	The aim of this study was to explore whether S. aureus strains isolated from AD skin (S. aureus - AD) were able to skew T cell responses via Langerhans cells (LC) as compared to a standard strain of S. aureus NCTC8325 or S. epidermidis. Monocyte-derived LC (MoLC) were prepared from peripheral blood of healthy controls and patients with AD. MoLC were stimulated with heat-inactivated S. aureus NCTC8325, S. aureus - AD, or S. epidermidis, respectively. After stimulation, CD1a-sorted MoLC were co-cultured with autologous CD4pos T cells and then T cell responses were analyzed. Compared to S. aureus NCTC8325 and S. epidermidis, MoLC stimulated by S. aureus - AD induced significantly high and rapid proliferation of T cells with significantly high amounts of IL-2 and less IFN-γ production. The mRNA from T cells after co-culture showed imbalanced Th1/Th2 (decreased TBX21/GATA3 ratio) expression. No significant differences were found on T cell responses against S. aureus between healthy controls and patients with AD. These data illustrate S. aureus - AD can skew T cell responses via LC toward imbalanced Th1 / Th2 skin immunity.

Staphylococcus aureus from atopic dermatitis skin alters cytokine production triggered by monocyte-derived Langerhans cell.