title: Increased lipopolysaccharide-induced tumour necrosis factor-alpha, interferon-gamma and interleukin-10 production in atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is based on a genetic predisposition, but environmental factors may trigger skin inflammation. According to the hygiene hypothesis, decreased exposure to microbial products in early childhood does not allow sufficient maturation of the immune system that is associated with an increased risk of atopic sensitization.
  
  
  OBJECTIVE
  The effect of lipopolysaccharide (LPS) on the cytokine production of peripheral blood mononuclear cells (PBMC) of AD patients and nonatopic controls was studied.
  
  
  METHODS
  PBMC were isolated from heparinized blood of 10 patients with AD and 10 nonatopic individuals, suspended in culture medium and stimulated with LPS. Cytokine levels in the supernatants were measured by immunoassays. Results Upon stimulation with LPS, PBMC from AD patients produced significantly higher amounts of tumour necrosis factor-alpha, interferon-gamma and interleukin (IL)-10 compared with control PBMC. LPS stimulation blocked the increased spontaneous production of IL-4 and IL-5 by PBMC from AD patients, but had no effect on IL-13 production.
  
  
  CONCLUSIONS
  These results demonstrate that the effects of LPS stimulation depend on both the type of cytokine and the origin of PBMC. Endotoxin exposure is suggested to modulate the disease course of AD.
authors.affiliation: Department of Dermatology, Inselspital, University of Bern, CH-3010 Bern, Switzerland. dagmar.simon@insel.ch
authors.forename: D
authors.initials: D
authors.lastname: Simon
authors.forename: L R
authors.initials: LR
authors.lastname: Braathen
authors.forename: H-U
authors.initials: HU
authors.lastname: Simon
mesh_terms: D000293:Adolescent; D000328:Adult; D002478:Cells, Cultured; D003876:Dermatitis, Atopic / Q000378:metabolism*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D017471:Receptors, Interferon / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D000096743:Interferon gamma Receptor
chemical_list: D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D053590:Interleukin 1 Receptor Antagonist Protein; D016753:Interleukin-10; D008070:Lipopolysaccharides; D017471:Receptors, Interferon; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D000096743:Interferon gamma Receptor; C507763:IL1RN protein, human