Abstract
Abstract Cutaneous inflammation is a recurrent manifestation of systemic lupus erythematosus (SLE), a severe autoimmune disease, and is triggered upon exposure to ultraviolet B (UVB) light. The exaggerated inflammatory response of SLE epidermis to UVB exposure is thought to be, in part, secondary to chronic exposure to type I interferons (IFN). S. aureus colonization has been found to stimulate cutaneous IFN. Indeed, our analysis of 54 SLE patients swabbed on their chest, nares and any active lesions demonstrated colonization of SLE patients at twice the rate (61%) of normal adult population (~30%). The rate increased further (67%) when active cutaneous lesions were sampled. We have also identified differences in expression of cutaneous IFN production in SLE patients, in particular IFNκ, and thus sought to investigate the role of IFNs in S. aureus adhesion to better define their impact on colonization. Immortalized keratinocytes (NTERTs), were grown to confluence, exposed to 20 mJ/cm2 UVB (310 nm) and 24hrs later exposed to ~107 cells of S. aureus. Following washing, the number of adherent cells were then determined by serial dilution and plating. Our results show that treatment with UVB increased S. aureus adhesion to WT-NTERTs. An increase in adhesion was observed in treatment of WT-NTERTs with 5ng/ml IFNα for 24 hours as well. NTERTs lacking IFNκ (IFNκ KO) unlike WT NTERTs exhibited lower S. aureus adhesion after UVB exposure which was reversed when functional IFNκ was added to growth media. These results suggest that increased IFN production in SLE skin may contribute to enhanced S. aureus colonization in these patients. The impact of S. aureus colonization on SLE skin remains to be determined.
Published Version
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