Cutaneous Na+ storage strengthens the antimicrobial barrier function of the skin and boosts macrophage-driven host defense

Cell Metab. 2015 Mar 3;21(3):493-501. doi: 10.1016/j.cmet.2015.02.003.

Abstract

Immune cells regulate a hypertonic microenvironment in the skin; however, the biological advantage of increased skin Na(+) concentrations is unknown. We found that Na(+) accumulated at the site of bacterial skin infections in humans and in mice. We used the protozoan parasite Leishmania major as a model of skin-prone macrophage infection to test the hypothesis that skin-Na(+) storage facilitates antimicrobial host defense. Activation of macrophages in the presence of high NaCl concentrations modified epigenetic markers and enhanced p38 mitogen-activated protein kinase (p38/MAPK)-dependent nuclear factor of activated T cells 5 (NFAT5) activation. This high-salt response resulted in elevated type-2 nitric oxide synthase (Nos2)-dependent NO production and improved Leishmania major control. Finally, we found that increasing Na(+) content in the skin by a high-salt diet boosted activation of macrophages in a Nfat5-dependent manner and promoted cutaneous antimicrobial defense. We suggest that the hypertonic microenvironment could serve as a barrier to infection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Infective Agents / pharmacology*
  • Enzyme Activation / physiology
  • Humans
  • Leishmania major / drug effects
  • Leishmaniasis, Cutaneous / drug therapy*
  • Leishmaniasis, Cutaneous / metabolism*
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Mice
  • NFATC Transcription Factors / metabolism
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Skin / drug effects
  • Skin / metabolism*
  • Sodium / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Anti-Infective Agents
  • NFATC Transcription Factors
  • Nitric Oxide
  • Sodium
  • Nitric Oxide Synthase Type II
  • p38 Mitogen-Activated Protein Kinases