Abstract
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.
Highlights
The interleukin 17 (IL-17) family comprises six subtypes (IL-17 A to F) which bind to homo- and hetero-dimeric receptor complexes of the IL-17 receptor family (IL-17RA to IL-RE) [1]
To study the function of the IL-17C/interleukin 17 receptor E (IL-17RE) axis in wound healing, punch wounds were introduced on both flanks of WT, Il-17c−/−, and Il-17re−/− mice, respectively, either infected with approximately 105 colony-forming units (CFU) of S. aureus strain Newman or treated with an equal volume of phosphate-buffered saline (PBS) as sham-infected control, and wound closure was monitored after day
We further demonstrated that the expression of IL-17C
Summary
The interleukin 17 (IL-17) family comprises six subtypes (IL-17 A to F) which bind to homo- and hetero-dimeric receptor complexes of the IL-17 receptor family (IL-17RA to IL-RE) [1]. IL-17C is mainly expressed by epithelial cells and mediates the expression of cytokines, chemokines, and antimicrobial peptides through a receptor complex of IL-17RA and IL-17RE, NF-kB, and MAP kinases [2,3,4]. Inflammatory mediators (e.g., TNF-α, IL1β) induce the expression of IL-17C in keratinocytes [2,3,5,6,7,8,9]. Ramirez-Carrozzi et al [3] demonstrated that IL-17C promotes imiquimod-dependent skin-inflammation, epidermal thickening, and keratinocyte proliferation. Studies have demonstrated that IL-17C is expressed in the skin of patients with atopic dermatitis, and that the treatment with therapeutic antibodies directed against IL-17C decreased skin inflammation in IL-23- and calcipotriol-dependent mouse models of psoriasis and atopic dermatitis, respectively [5,6,8]
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