Inflammation requires metabolic reprogramming of monocytes and macrophages to support immune responses, such as the synthesis of the proinflammatory cytokine IL-1β. Kimshowed that intracellular zinc ions promoted a metabolic shift in human monocytes and macrophages that enhanced IL-1β production. Zinc influx into monocytes and macrophages required the expression of the gene encoding the transporter Zip8.
Here, we demonstrated that cytoplasmic, bioavailable zinc was essential for promoting IL-1β production in activated human monocytes and macrophages downstream of glycolysis induced by the kinase-containing multiprotein complex mTORC1. The concentration of cytoplasmic zinc was determined by that of extracellular zinc, which was brought into cells through the zinc-specific importer Zip8.
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