title: Interleukin-18 is elevated in the horny layer in patients with atopic dermatitis and is associated with Staphylococcus aureus colonization.
abstract: BACKGROUND
  An increase in interleukin (IL)-18 production from epidermal cells has been reported in an atopic dermatitis (AD) mouse model, and subsequent topical application of Staphylococcus aureus results in severe dermatitis.
  
  
  OBJECTIVE
  To reveal the relationship between S. aureus colonization of skin lesions and keratinocyte IL-18 production, particularly in AD with relatively low serum IgE levels. We also aimed to establish a simple and noninvasive method of assaying IL-18 produced by epidermal keratinocytes to evaluate local skin inflammation and therapeutic effects in patients with AD.
  
  
  METHODS
  IL-18 in the horny layer of the skin was collected via a tape-stripping method and measured in 95 patients with AD and 40 healthy controls by enzyme-linked immunosorbent assay (ELISA). Clinical severity, blood data and S. aureus skin colonization were evaluated before and after treatment.
  
  
  RESULTS
  IL-18 levels in the horny layer were significantly higher in the skin lesions of patients with AD than in healthy controls and correlated with SCORAD, levels of serum IL-18, IgE, lactate dehydrogenase, thymus and activation-regulated chemokine, blood eosinophils and transepidermal water loss. In the AD group with serum IgE < 1500 IU mL(-1) , significantly higher IL-18 levels were observed in the horny layer of patients colonized with S. aureus compared with those who were not.
  
  
  CONCLUSIONS
  Epidermal IL-18 production was associated with the severity of AD. Staphylococcus aureus colonization seems to contribute to this IL-18 production, especially in the AD group with relatively low IgE production. Tape stripping provides an easy and noninvasive method to assess epidermal IL-18 production by ELISA.
authors.affiliation: Department of Environmental Immuno-Dermatology and Department of Molecular Pathology, Yokohama City University Graduate School of Medicine, Kanazawa-ku, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Aihara
authors.forename: M
authors.initials: M
authors.lastname: Kirino
authors.forename: I
authors.initials: I
authors.lastname: Harada
authors.forename: J
authors.initials: J
authors.lastname: Komori-Yamaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Nagashima
authors.forename: Z
authors.initials: Z
authors.lastname: Ikezawa
mesh_terms: D000328:Adult; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000382:microbiology* / Q000503:physiopathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020382:Interleukin-18 / Q000096:biosynthesis*; D015603:Keratinocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013203:Staphylococcal Infections / Q000276:immunology*; D013211:Staphylococcus aureus; D014870:Water Loss, Insensible; D055815:Young Adult
chemical_list: D020382:Interleukin-18