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ROSA-Award "Atopic Dermatitis", La Roche-Posay, 2016, for SFB 1112 Publication

News from Jul 05, 2016

For their excellent research work in the field of Atopic Dermatitis, Prof. Dr. Sarah Hedtrich and co-authors received this year's "Research on Skin-Dryness Award (R.O.S.A)".

The R.O.S.A.-Prize 2016 in the field of "Atopic Dermatitis" was awarded for the SFB 1112-publication "Influence of Th2 cytokines on the cornified envelope, tight junction proteins and ß-defensins in filaggrin-deficient skin models" by Stefan Hönzke, Leonie Wallmeyer, Anja Ostrowski, Moritz Radbruch, Lars Mundhenk, Monika Schäfer-Korting and Sarah Hedtrich (J Invest Dermatol 136:631-639, 2015).

Atopic dermatitis is a chronic skin condition with complex etiology. It is characterized by skin barrier defects and T helper type 2 (Th2)-polarized inflammation. Although mutations in the filaggrin gene are known to be prominent genetic risk factors for the development of atopic dermatitis, the interdependency between these and an altered cytokine milieu is not fully understood.In this study, we evaluated the direct effects of filaggrin deficiency on the cornified envelope, tight junction proteins, and innate immune response, and report the effects of Th2 cytokines in normal and filaggrin-deficient skin equivalents. Supplementation with IL-4 and IL-13 led to distinct histologic changes and significantly increased skin surface pH, both of which were enhanced in filaggrin knockdown skin equivalents. We detected a compensatory up-regulation of involucrin and occludin in filaggrin-deficient skin that was dramatically disturbed when simultaneous inflammation occurred. Furthermore, we found that a lack of filaggrin triggered an up-regulation of human β-defensin 2 via an unknown mechanism, which was abolished by Th2 cytokine supplementation.Taken together, these results indicate that defects in the epidermal barrier, skin permeability, and cutaneous innate immune response are not primarily linked to filaggrin deficiency but are rather secondarily induced by Th2 inflammation.

The prize-winning study results from cooperative work of SFB 1112-groups at the Institute of Pharmacy (Project C02: In vitro disease models - test platform for the investigation of nanocarrier related transport, activity, and toxicity of drugs; Prof. Dr. Monika Schäfer-Korting and Prof. Dr. Sarah Hedtrich) and at the Institute of Veterinary Pathology (Projekt C03: Nanocarriers in the skin of mouse models: Penetration, effects of barrier dysfunction in deseased skin and improved targeting of inflammation; Prof. Dr. Achim Gruber und Dr. Lars Mundhenk) at Freie Universität Berlin.

The prize is awarded by Fondation La Roche-Posay and carries a value of 8.000 Euro. The award was presented in the frame of the 25th Continuing Education Week on Applied Dermatology and Venerology Seminar "Hot Topics Atopic Dermatitis - Psoriasis" on July 26, 2016 in Munich.

SFB 1112 congratulates Prof. Hedtrich and all involved SFB-members!

Awarded Publication:
Hönzke S, Wallmeyer L, Ostrowski A, Radbruch M, Mundhenk L, Schäfer-Korting M, Hedtrich S 2015. Influence of Th2 cytokines on the cornified envelope, tight junction proteins and ß-defensins in filaggrin-deficient skin models. J Invest Dermatol 136:631-639 DOI 10.1016/j.jid.2015.11.007

More information:
(German only)

"Die Gene sind nicht schuld" - Freie Universität Berlin, Stabsstelle Presse und Kommunikation, Wissenschaft aktuell, 2016, Themen im September
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