| Summary: | The epithelial cytokine interleukin-17C (IL-17C) mediates inflammation through the interleukin 17 receptor E (IL-17RE). Prior studies showed a detrimental role of IL-17C in the pathogenesis of immune-mediated skin diseases (e.g., psoriasis). Here, we examined the role of IL-17C/IL-17RE in wound closure in a <i>Staphylococcus aureus</i> wound infection model. We demonstrate that wound closure is significantly delayed in IL-17RE (<i>Il-17re<sup>−/−</sup></i>)- and 17C (<i>Il-17c<sup>−/−</sup></i>)-deficient mice. There was no significant difference between WT, <i>Il-17re<sup>−/−</sup></i>, and <i>Il-17c<sup>−/−</sup></i> mice in the absence of infection. Deficiency for IL-17RE and IL-17C did not significantly affect the elimination of bacteria. IL-17C expression was increased in the epidermis of human <i>S. aureus</i>-infected skin. Our results indicate that the IL-17C/IL-17RE axis contributes to the closure of infected wounds but does not contribute to the elimination of <i>S. aureus</i>.
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