Other - Immunology and metabolism
High salt intake has been associated with shifts in the immune cell balance, mainly by promoting proliferation and activity of pro-inflammatory cells, such as T helper 17 (Th17) and M1 macrophages, and by impairing the functions of anti-inflammatory cells such as regulatory T cells (Tregs) and M2 macrophages. However, the precise molecular mechanisms that lead to this phenotype are still unknown. The role of metabolic regulation in shaping immune responses has gained increasing attention in recent years. Cellular metabolism is a vital process, which is essential for growth, survival and proliferation of every cell type, and can be greatly influenced by environmental factors such as diet. Previous studies have shown that high-salt leads to metabolic changes in M2 macrophages by decreasing their mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis necessary for their activation. Here we analyzed the effect of high-salt on cellular metabolism of human Tregs. Of note, our results show significant salt-induced changes in metabolism of human Tregs. Since these changes are known to alter Treg suppressive function both in vitro and in vivo, we hypothesize that the observed metabolic alterations might be linked to the loss of suppressive function seen in human Tregs upon high-salt challenge. Thus, the interference with these pathways may have the potential for targeting Tregs in salt-sensitive diseases.