Staphylococcus aureus and toll-like receptor activity in atopic dermatitis

Introduction Staphylococcus aureus skin infections is an almost ubiquitous feature of patients with atopic dermatitis (AD). TLR1, 2 and 6 are important in immune sensing of these bacteria. The aim of this study was to determine whether defects in TLR1, 2 and/or 6 expression / function may explain the propensity to infection in humans and the NC eczema mouse model.Methods Fibroblast cell lines from severe AD, nonatopic controls, and mouse embryonic fibroblasts (MEFs) from the NC, MSM/Ms wild-type strain and a 3T3 control strain TLR1, 2 and 6 expression were measured by qPCR and FACS. IL-6, TNF-α, TSLP and IL-33 production was measured by qPCR and ELISA at baseline and after stimulation with LPS, HKSA and a live strain of Staphylococcus aureus that produced only SEB. Results No differences were found in either TLR expression or function in human fibroblasts derived from patients and controls. The MSM/Ms MEFs expressed significantly more TLR1 and 2, as well as exhibited high inflammatory profile after stimulation comparing with 3T3 and the NC MEFs. Live Staphylococcus aureus, but not HKSA, LPS or SEB, was a potent stimulus for the Th2-inducing cytokines (TSLP and IL-33), and induce cell death. Cytokines levels were found to be similar in AD and NC MEFs when compared to healthy controls. Conclusion Eczema in both the human and NC mouse is not associated with abnormalities in fibroblasts TLR1, 2, and 6. Live, but not killed Staphylococcus aureus or its enterotoxin, is a potent inducer of TSLP and IL-33 in both species.