Recent animal studies, as well as quantitative sodium MRI observations on humans demonstrated
that remarkable amounts of sodium can be stored in the skin. It is also known that
excess sodium in the tissues leads to inflammation in various organs, but its role
in dermal pathophysiology has not been elucidated. Therefore, our aim was to study
the effect of dietary salt loading on inflammatory process and related extracellular
matrix (ECM) remodeling in the skin. To investigate the effect of high salt consumption
on inflammation and ECM production in the skin mice were kept on normal (NSD) or high
salt (HSD) diet and then dermatitis was induced with imiquimod (IMQ) treatment. The
effect of high salt concentration on dermal fibroblasts (DF) and peripheral blood
mononuclear cells (PBMC) was also investigated in vitro.
The HSD resulted in increased sodium content in the skin of mice. Inflammatory cytokine
Il17 expression was elevated in the skin of HSD mice. Expression
of anti-inflammatory Il10 and Il13
decreased in the skin of HSD or HSD IMQ mice. The fibroblast marker Acta2
and ECM component Fn and Col1a1
decreased in HSD IMQ mice. Expression of ECM remodeling related Pdgfb
and activation phosphorylated (p)-SMAD2/3 was lower in HSD IMQ mice. In PBMCs, production
of IL10, IL13 and PDGFB
was reduced due to high salt loading. In cultured DFs high salt concentration resulted
in decreased cell motility and ECM production, as well. Our results demonstrate that
high dietary salt intake is associated with increased dermal pro-inflammatory status.
Interestingly, although inflammation induces the synthesis of ECM in most organs,
the expression of ECM decreased in the inflamed skin of mice on high salt diet. Our
data suggest that salt intake may alter the process of skin remodeling.
