title: Skin barrier impairment correlates with cutaneous Staphylococcus aureus colonization and sensitization to skin-associated microbial antigens in adult patients with atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a chronic inflammatory skin disease. The pathogenesis of AD involves skin barrier defects and dysregulation of innate and adaptive immunity. Some environmental factors such as stress, infections, and allergens are associated with aggravation of AD. The aim of the study was to investigate the relationship between skin barrier function, skin colonization of Staphylococcus aureus, and sensitization to antigens of skin-associated microorganisms in adult patients with AD.
  
  
  METHODS
  Thirty adult patients with AD and 10 controls were recruited. Eczema severity was assessed, and transepidermal water loss (TEWL) was measured. Bacterial samples were taken from the skin using a swab technique for qualitative identification of S. aureus and a contact agar disc method for quantitative assessment. Immunological analyses of specific IgE to staphylococcal enterotoxins and yeasts as well as total serum IgE levels, were performed.
  
  
  RESULTS
  TEWL was significantly higher among S. aureus-positive patients in comparison to S. aureus-negative patients with AD (P < 0.05). TEWL increased with increasing bacterial load (P = 0.018). In the group of patients sensitized to all three of the investigated skin-associated microorganisms (S. aureus, Malassezia, and Candida), an increased TEWL was observed, in comparison to patients sensitized to none, or one or two (P = 0.026).
  
  
  CONCLUSIONS
  In adult patients with AD, a disrupted skin barrier promotes skin colonization by microbes, such as S. aureus. Heavy microbial colonization may facilitate skin penetration of microbial antigens leading to subsequent IgE sensitization. These results illustrate the importance of skin-associated microbial colonization and sensitization to microbial-derived allergens in eczema pathogenesis.
authors.affiliation: Division of Dermatology and Venereology, Department of Clinical Sciences, Lund University, Lund, Sweden.
authors.forename: Camilla Ling
authors.initials: CL
authors.lastname: Jinnestål
authors.forename: Emma
authors.initials: E
authors.lastname: Belfrage
authors.forename: Ove
authors.initials: O
authors.lastname: Bäck
authors.forename: Artur
authors.initials: A
authors.lastname: Schmidtchen
authors.forename: Andreas
authors.initials: A
authors.lastname: Sonesson
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012867:Skin / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013207:Staphylococcal Skin Infections / Q000276:immunology* / Q000473:pathology*; D013211:Staphylococcus aureus / Q000254:growth & development / Q000276:immunology*; D055815:Young Adult
chemical_list: D000942:Antigens, Bacterial