IL-17C and IL-17RE Promote Wound Closure in a <i>Staphylococcus aureus</i>-Based Murine Wound Infection Model

• Main Authors: Linda Pätzold, Alexandra Stark, Felix Ritzmann, Carola Meier, Thomas Tschernig, Jörg Reichrath, Robert Bals, Markus Bischoff, Christoph Beisswenger
• Format: Article
• Language: English
• Published: MDPI AG 2021-08-01
• Series: Microorganisms
• Subjects: <i>Staphylococcus aureus</i>; wound infection; interleukin-17C; wound closure
• Online Access: https://www.mdpi.com/2076-2607/9/9/1821

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^−/−</i>)- and 17C (<i>Il-17c^−/−</i>)-deficient mice. There was no significant difference between WT, <i>Il-17re^−/−</i>, and <i>Il-17c^−/−</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>.