| Abstrakt: |
Staphylococcus epidermidis is a commensal on skin, whereas Staphylococcus aureus is a transient pathogen. The aim was to determine whether the skin's innate defence systems responded differently to these microorganisms. Differential gene expression of a human skin equivalent (SE) model was assessed by microarray technology, in response to colonization by S. epidermidis or S. aureus. Only a small number of transcripts were significantly ( P<0.0001) increased (12) or decreased (35) with gene expression changes of >2-fold on SEs colonized with S. epidermidis compared with controls (no colonization). Expression of one innate defence gene, pentraxin 3 (PTX3), was upregulated, while psoriasin, S100A12, S100A15, β defensin 4, β defensin 3, lipocalin 2 and peptidoglycan recognition protein 2 were downregulated. In contrast, large numbers of transcripts were significantly increased (480) or decreased (397) with gene expression changes of >2-fold on SEs colonized with S. aureus compared with controls. There was upregulation in gene expression of many skin defence factors including Toll-like receptor 2, β defensin 4, properdin, PTX3, proinflammatory cytokines tumour necrosis factor-α, IL-1α, IL-1β, IL-17C, IL-20, IL-23A and chemokines IL-8, CCL4, CCL5, CCL20 and CCL27. These differences may partly explain why S. epidermidis is a normal skin resident and S. aureus is not. [ABSTRACT FROM AUTHOR] |
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