Dendritic cells produce inflammatory cytokines in response to bacterial products from Staphylococcus aureus-infected atopic dermatitis lesions.

Atopic Dermatitis (AD) patients often acquire secondary skin infections resulting in increased inflammation. The increased inflammation occurs through the activation of multiple cell types including dendritic cells (DC). In this study, we investigated the activity of soluble products present in infected AD lesions by measuring the ability of patients' wash fluids from a quantitative culture of lesions to activate DC. We found that wash fluid derived from AD lesions induced cytokine production by murine bone marrow-derived DC, including IL-1β, IL-6, ΙL-10, and tumor necrosis factor-α. The lipoprotein lipoteichoic acid (LTA) from Staphylococcusaureus was implicated as a potent stimulus in the wash fluids as only wash fluid samples that contained LTA exerted this activity, and exogenous LTA triggered similar DC cytokine activation. Wash fluid- and LTA-stimulated DC cytokine production required MyD88, but not the platelet-activating factor receptor (PAF-R), despite the ability of LTA to function through this receptor in keratinocytes. Thus, our results support a role for DC in the worsening of AD inflammation due to secondary bacteria infections.