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IL-17C and IL-17RE Promote Wound Closure in a Staphylococcus aureus-Based Murine Wound Infection Model.

Linda PätzoldAlexandra StarkFelix RitzmannCarola MeierThomas TschernigJörg ReichrathRobert BalsMarkus BischoffChristoph Beisswenger
Published in: Microorganisms (2021)
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 Staphylococcus aureus wound infection model. We demonstrate that wound closure is significantly delayed in IL-17RE (Il-17re-/-)- and 17C (Il-17c-/-)-deficient mice. There was no significant difference between WT, Il-17re-/-, and Il-17c-/- 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 S. aureus-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 S. aureus.
Keyphrases
  • staphylococcus aureus
  • oxidative stress
  • type diabetes
  • endothelial cells
  • metabolic syndrome
  • adipose tissue
  • cystic fibrosis
  • skeletal muscle
  • pseudomonas aeruginosa
  • pluripotent stem cells