The Biological Advantage of Common Salt (NaCl) Intake
Human diet with salt is the primary source of Na+ (sodium ion) in the body. Na+ metabolism may represent an unappreciated functional component of skin barrier formation. Large amounts of Na+ are stored in the skin. The researches suggests that skin Na+ deposition is linked with disease in humans (primary (essential) and secondary hypertension, inflammation and even carcinogenesis).
The biological advantage of Na+ storage is unknown. Authors speculate that an underlying biological principle of Na+ metabolism is to generate hypertonic microenvironments as a protective element against outside invaders.
Using a mouse model, authors report the following findings:
1. Infection Increases Na+ Storage in Skin: Using 23Na MRI, the authors report that infected areas displayed remarkable Na+ accumulation, which was reduced after antibiotic treatment.
2. NaCl Boosts macrophages (MF) Activation: A 40 mM increase in culture medium NaCl concentration (HS) boosted LPS-triggered induction of Nos2 on mRNA and protein level with enhanced NO release in RAW 264.7 MF and bone-marrow-derived MF (BMM). Moreover, they found that this rise in macrophages is via the p38/MAPK signaling cascade.
3. HSD Ameliorates Cutaneous L. Major Infection In Vivo: To test the hypothesis that high salt diet (HSD) may promote the healing of hind footpad infection with L. Major, two sets of mice were selected. Within the first 20 days after infection, footpad thickness increased in mice fed either low-salt diet (LSD) or HSD. LSD mice then showed a non-resolving course of infection with persistent skin lesions, whereas the footpad thickness steadily decreased in HSD mice. Improved healing was paralleled by increased (Na+ + K+)/water ratio in HSD mice.
The authors conclude that dietary salt bears a therapeutic potential to promote anti-microbial barrier function of the skin.
Article citation: Jantsch, J.; et. al. Cutaneous Na+ Storage Strengthens the Antimicrobial Barrier Function of the Skin and Boosts Macrophage-Driven Host Defense. Cell Metabolism DOI: http://dx.doi.org/10.1016/j.cmet.2015.02.003
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