IL-22 derived from γδ T cells restrictsStaphylococcus aureusinfection of mechanically injured skin

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Staphylococcus aureusis an opportunistic pathogen that colonizes the skin of patients with atopic dermatitis (AD) and aggravates their disease. Neutrophils and the cytokines IL-17A and IL-17F, which drive the expression of the neutrophil-attracting chemokines, are important for the clearance ofS aureusinfection. The cytokine IL-22 is often coproduced by IL-17–secreting cells. The levels of IL-22 are elevated in AD skin lesions.


We sought to determine the role of IL-22 in the clearance ofS aureusinfection of mouse skin subjected to tape stripping, a surrogate for scratching, a cardinal feature of AD.


S aureuswas applied to the tape-stripped skin of wild-type andIl22−/−mice. Bacterial burden was evaluated by enumerating colony-forming units. Quantitative PCR and ELISA were performed to quantifyIl22mRNA and IL-22 protein in mouse and human skin. Flow cytometry was used to enumerate neutrophils in the skin.


Scratching the skin of healthy adults and tape stripping of mouse skin induced local expression ofIl22mRNA and IL-22 protein. Induction ofIl22expression by tape stripping was dependent on IL-23 and γδ T cells. Clearance ofS aureusfrom tape-stripped skin was significantly impaired inIl22−/−mice. Neutrophil infiltration and upregulation of expression of genes encoding the antimicrobial peptides antigen-6/urokinase-type plasminogen activator receptor related protein-1 and β-DEFENSIN 14 and the chemokine (C-X-C motif) ligand following tape stripping were significantly impaired inIl22−/−mice.


These findings show that IL-22 is important for limiting the growth ofS aureuson mechanically injured skin and caution that IL-23 and IL-22 blockade in patients with AD may enhance susceptibility to staphylococcal skin infection.

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