Skin sodium accumulates in psoriasis and reflects disease severity

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.