Expression of the sweat‐derived innate defence antimicrobial peptide dermcidin is not impaired in Staphylococcus aureus colonization or recurrent skin infections. (20th June 2013)

• Record Type: Journal Article
• Authors: Rieg, S.; Saborowski, V.; Kern, W. V.; Jonas, D.; Bruckner‐Tuderman, L.; Hofmann, S. C.
• Is Part Of: Clinical and experimental dermatology. Volume 39:Number 2(2014)
• Page Start: 209
• Page End: 212
• Publication Date: 2013-06-20
• Subjects: Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/ced.12189
• Languages: English
• ISSNs: 0307-6938

Abstract

<abstract abstract-type="main" id="ced12189-abs-0001"> <title>Summary</title> <p>Antimicrobial peptides are an integral part of innate immunity, and contribute to the protection of human skin from <italic>Staphylococcus aureus</italic> colonization and infection. We sought to investigate whether the expression of the eccrine sweat‐derived staphylocidal antimicrobial peptide dermcidin might influence <italic>S. aureus</italic> colonization or recurrent skin and soft‐tissue infections (SSTIs). Eccrine sweat was collected from 18 patients with recurrent <italic>S. aureus </italic>SSTIs, 28 patients who were intermittent or permanent <italic>S. aureus</italic> carriers, and 32 noncarriers. Expression and proteolytic degradation of dermcidin was investigated using ELISA and surface‐enhanced laser desorption ionization time‐of‐flight mass spectrometry (SELDI‐TOF‐MS). We found no significant differences in the overall amount or the proteolytic degradation pattern of dermcidin‐derived peptides between healthy noncarriers, intermittent and permanent carriers, and patients with recurrent <italic>S. aureus </italic>SSTIs. <italic>S. aureus</italic> colonization or recurrent SSTIs do not seem to be associated with diminished dermcidin expression in eccrine sweat.</p> </abstract>