Please use this identifier to cite or link to this item: doi:10.22028/D291-34762
Title: IL-17C and IL-17RE Promote Wound Closure in a Staphylococcus aureus-Based Murine Wound Infection Model
Author(s): Pätzold, Linda
Stark, Alexandra
Ritzmann, Felix
Meier, Carola
Tschernig, Thomas
Reichrath, Jörg
Bals, Robert
Bischoff, Markus
Beisswenger, Christoph
Language: English
Title: Microorganisms
Volume: 9
Issue: 9
Publisher/Platform: MDPI
Year of Publication: 2021
Free key words: Staphylococcus aureus
wound infection
interleukin-17C
wound closure
DDC notations: 610 Medicine and health
Publikation type: Journal Article
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.
DOI of the first publication: 10.3390/microorganisms9091821
Link to this record: urn:nbn:de:bsz:291--ds-347628
hdl:20.500.11880/31801
http://dx.doi.org/10.22028/D291-34762
ISSN: 2076-2607
Date of registration: 27-Sep-2021
Faculty: M - Medizinische Fakultät
Department: M - Anatomie und Zellbiologie
M - Dermatologie
M - Infektionsmedizin
M - Innere Medizin
Professorship: M - Prof. Dr. Robert Bals
M - Prof. Dr. Dr. Sören Becker
M - Prof. Dr. Carola Meier
M - Keiner Professur zugeordnet
Collections:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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