Edited by: Hans-Uwe Simon
Long-term reduction in local inflammation by a lipid raft molecule in atopic dermatitis
Version of Record online: 10 MAR 2010
© 2010 John Wiley & Sons A/S
Volume 65, Issue 9, pages 1158–1165, September 2010
How to Cite
Dölle, S., Hoser, D., Rasche, C., Loddenkemper, C., Maurer, M., Zuberbier, T. and Worm, M. (2010), Long-term reduction in local inflammation by a lipid raft molecule in atopic dermatitis. Allergy, 65: 1158–1165. doi: 10.1111/j.1398-9995.2010.02341.x
- Issue online: 4 AUG 2010
- Version of Record online: 10 MAR 2010
- Accepted for publication 15 January 2010
- atopic dermatitis;
- regulatory T cell;
- thermographic imaging
To cite this article: Dölle S, Hoser D, Rasche C, Loddenkemper C, Maurer M, Zuberbier T, Worm M. Long-term reduction in local inflammation by a lipid raft molecule in atopic dermatitis. Allergy 2010; 65: 1158–1165.
Background: The complex pathogenesis of atopic dermatitis (AD) is guided by cell surface receptor-mediated signal transduction regulated in lipid rafts. Miltefosine is a raft-modulating molecule targeting cell membranes. With this controlled clinical study, the clinical and immunomodulatory efficacy of miltefosine was investigated in patients with AD in comparison with a topical corticosteroid treatment.
Methods: Sixteen patients with AD were treated topically with miltefosine and hydrocortisone localized on representative AD target lesions for 3 weeks. To assess the clinical efficacy, the three item severity (TIS) score was evaluated before, during and after treatment as well as after 4-week-follow-up period. To study the anti-inflammatory effect of miltefosine on the cellular T cell pattern, skin biopsies were analysed before and after treatment.
Results: The TIS score dropped in both groups significantly after treatment. A carry-over effect was exclusively seen for miltefosine after discontinuing the treatment. These findings were substantiated by thermographic imaging with a significant decrease in the maximum temperature (Tmax) after miltefosine application (P = 0.034, ΔTmax = 1.7°C [2.1–3.9]). Immunohistochemically, a reduction in lesional CD4+-infiltrating T cells was observed in both treatments. Moreover, increased FoxP3+ cells were present in the skin after miltefosine treatment (before 5.4% [1.9–9.8], after 6.2% [3.5–9.5]).
Conclusion: We demonstrate that miltefosine is locally active in patients with AD and led to a sustained clinical improvement in local skin inflammation. Moreover, the increased frequency of FoxP3+ cells in the skin of patients with AD suggests its immunomodulatory properties.