Skin sodium accumulates in psoriasis and reflects disease severity
Authors
- A. Maifeld
- J. Wild
- T.V. Karlsen
- N. Rakova
- E. Wistorf
- P. Linz
- R. Jung
- A. Birukov
- V.A. Gimenez-Rivera
- N. Wilck
- T. Bartolomaeus
- R. Dechend
- M. Kleinewietfeld
- S.K. Forslund
- A. Krause
- G. Kokolakis
- S. Philipp
- B.E. Clausen
- A. Brand
- A. Waisman
- F.C. Kurschus
- J. Wegner
- M. Schultheis
- F.C. Luft
- M. Boschmann
- M. Kelm
- H. Wiig
- T. Kuehne
- D.N. Müller
- S. Karbach
- L. Markó
Journal
- Journal of Investigative Dermatology
Citation
- J Invest Dermatol 142 (1): 166-178
Abstract
Sodium can accumulate in the skin, at concentrations exceeding serum levels. High sodium environment can lead to pathogenic T helper (Th)17 cell expansion. Psoriasis is a chronic inflammatory skin disease in which interleukin (IL)-17-producing Th17 cells play a crucial role. In an observational study, we measured skin sodium content in psoriasis patients and age-matched healthy controls by (23)Na-magnetic resonance imaging (MRI). Patients with a psoriasis area and severity index (PASI)>5 showed significantly higher sodium and water content in the skin, but not in other tissues, compared to those with lower PASI or healthy controls. Skin sodium concentrations measured by (23)Na-spectroscopy or by atomic adsorption spectrometry in ashed-skin biopsies verified findings with (23)Na-MRI. In vitro Th17 cell differentiation of naïve CD4(+) cells from psoriatic patients markedly induced IL-17A expression under increased NaCl concentrations. The imiquimod-induced psoriasis mouse model replicated the human findings. Extracellular tracer (51)Cr-EDTA measurements in imiquimod- and sham-treated skin showed similar extracellular volumes, rendering excessive water of intracellular origin. Chronic genetic IL-17A-driven psoriasis mouse models underlined the role of IL-17A in dermal sodium accumulation and inflammation. Our data describe skin sodium as a pathophysiological feature of psoriasis, which could open new avenues for its treatment.