Changes of antimicrobial peptide mRNA expression in atopic eczema following phototherapy.

Autor: Gambichler T; Department of Dermatology, Ruhr-University of Bochum, Gudrunstr 56, Bochum, Germany. t.gambichler@klinikum-bochum.de, Skrygan M, Tomi NS, Altmeyer P, Kreuter A
Jazyk: angličtina
Zdroj: The British journal of dermatology [Br J Dermatol] 2006 Dec; Vol. 155 (6), pp. 1275-8.
DOI: 10.1111/j.1365-2133.2006.07481.x
Abstrakt: Background: The epidermal expression of antimicrobial peptides (AMPs) such as human beta-defensin (hBD)-2 and cathelicidin LL-37 is downregulated in atopic eczema (AE) as compared with psoriasis. Hence, AMPs may represent important cofactors in the pathogenesis of AE.
Objectives: In the present pilot study we aimed to investigate whether the cutaneous mRNA expression of AMPs is altered in patients with AE following narrowband ultraviolet B (NB-UVB) phototherapy.
Methods: We studied 12 patients diagnosed with extrinsic AE who underwent a 6-week course of NB-UVB. Skin biopsies were taken from healthy controls (n = 12) and patients with AE at baseline and after the last NB-UVB irradiation. Quantitative real-time reverse transcription-polymerase chain reaction was performed for hBD-1, hBD-2, hBD-3 and LL-37.
Results: A significant (P < 0.05) reduction in the clinical score was observed after treatment with NB-UVB. As compared with controls, patients with AE showed a significantly lower hBD-1 mRNA expression and significantly higher hBD-2 levels (P < 0.05). Following NB-UVB treatment of patients with AE we observed a significant increase of hBD-1 expression as well a significant decrease of hBD-2 (P < 0.05). Levels of hBD-3 and LL-37 did not significantly differ between the groups (P > 0.05).
Conclusions: The pattern of mRNA expression of constitutive (hBD-1) as well as inducible (hBD-2) AMPs seems to be altered in AE as compared with healthy controls. The resolution of AE lesions following phototherapy is accompanied by significant changes in mRNA expression of hBDs, indicating that AMPs may play a role in the pathogenesis of AE.
Databáze: MEDLINE
Externí odkaz: