Salt increases monocyte CCR2 expression and inflammatory responses in humans

Area of Science:

• Immunology
• Cardiovascular Research
• Nutrition Science

Background:

• High salt intake is linked to adverse health outcomes, with inflammation suspected as a mediating factor.
• The specific effects of salt on human monocyte and macrophage inflammatory priming remain largely uncharacterized.

Purpose of the Study:

• To investigate the in vitro and in vivo effects of salt on human monocyte and macrophage inflammatory responses.
• To determine if dietary salt modulates monocyte infiltration and macrophage phenotype.

Main Methods:

• A randomized crossover trial involving 11 healthy subjects on controlled low-salt and high-salt diets for 2 weeks each.
• Analysis of monocyte CCR2 expression, plasma MCP-1 levels, monocyte transendothelial migration, and skin macrophage density.
• Assessment of macrophage proinflammatory phenotype via LPS-induced cytokine secretion (IL-6, TNF, IL-10) and surface marker expression (HLA-DR, CD206).

Main Results:

• High salt intake significantly increased monocyte CCR2 expression and plasma MCP-1 levels.
• Salt exposure led to increased monocyte transendothelial migration and higher skin macrophage density.
• Macrophages exhibited an enhanced proinflammatory phenotype, with boosted LPS-induced cytokine release and altered surface marker expression (increased HLA-DR, decreased CD206).

Conclusions:

• Dietary salt can induce proinflammatory priming of monocytes and macrophages in humans.
• These salt-induced inflammatory changes in immune cells may contribute to the detrimental health effects associated with high salt consumption.
• Targeting salt-induced inflammation presents a potential therapeutic avenue for mitigating high salt intake's adverse consequences.