Conflicts of interest None declared.
Increased lipopolysaccharide-induced tumour necrosis factor-α, interferon-γ and interleukin-10 production in atopic dermatitis
Article first published online: 26 JUN 2007
British Journal of Dermatology
Volume 157, Issue 3, pages 583–586, September 2007
How to Cite
Simon, D., Braathen, L.R. and Simon, H.-U. (2007), Increased lipopolysaccharide-induced tumour necrosis factor-α, interferon-γ and interleukin-10 production in atopic dermatitis. British Journal of Dermatology, 157: 583–586. doi: 10.1111/j.1365-2133.2007.08050.x
- Issue published online: 10 AUG 2007
- Article first published online: 26 JUN 2007
- Accepted for publication 1 March 2007
- atopic dermatitis;
- tumour necrosis factor-α;
- toll-like receptor 4
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.
Objectives The effect of lipopolysaccharide (LPS) on the cytokine production of peripheral blood mononuclear cells (PBMC) of AD patients and nonatopic controls was studied.
Patients and 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-α, interferon-γ 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.