title: Differential innate immune responses of a living skin equivalent model colonized by Staphylococcus epidermidis or Staphylococcus aureus.
abstract: 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, beta defensin 4, beta 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, beta defensin 4, properdin, PTX3, proinflammatory cytokines tumour necrosis factor-alpha, IL-1 alpha, IL-1 beta, 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.
authors.affiliation: Skin Research Centre, Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
authors.forename: Diana B
authors.initials: DB
authors.lastname: Holland
authors.forename: Richard A
authors.initials: RA
authors.lastname: Bojar
authors.forename: Mark D
authors.initials: MD
authors.lastname: Farrar
authors.forename: Keith T
authors.initials: KT
authors.lastname: Holland
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D023082:Defensins / Q000235:genetics / Q000276:immunology; D005347:Fibroblasts / Q000276:immunology / Q000382:microbiology; D015870:Gene Expression; D006801:Humans; D007113:Immunity, Innate; D015603:Keratinocytes / Q000276:immunology / Q000382:microbiology; D008954:Models, Biological; D000683:Serum Amyloid P-Component / Q000235:genetics / Q000276:immunology; D012867:Skin / Q000276:immunology* / Q000382:microbiology*; D013203:Staphylococcal Infections / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000254:growth & development* / Q000276:immunology; D013212:Staphylococcus epidermidis / Q000254:growth & development* / Q000276:immunology; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D016207:Cytokines; D023082:Defensins; D000683:Serum Amyloid P-Component; D000099153:Pentraxins