Cytoplasmic labile zinc regulates IL-1β production in human monocytes/macrophages via mTORC1-induced glycolysis

• DOI: 10.4049/jimmunol.204.supp.226.24
• Publication Date: 2023-01-01T14:33:41Z
• Authors: Bonah Kim; Su Jeong Lee; Yeon Jun Kang; Ga Hye Lee; Hee Young Kim; Won-Woo Lee
• Keywords: Proinflammatory cytokine; Monocyte

Abstract Zinc is an essential micronutrient that plays critical roles in multiple facets of biological processes, including growth, development, proliferation, and differentiation. Since dysregulated zinc homeostasis impairs overall immune function resultantly, increases susceptibility to infection, much attention has been recently paid immunomodulatory cells. Rapid efficient production proinflammatory cytokines, such as IL-1β TNF-α, a primary effect monocytes/macrophages for host defense. However, the molecular mechanism involved with zinc-mediated modulation cytokine needs be better understood. In present study, we provide evidence cytoplasmic labile human via mTORC1-induced glycolysis. We found level was largely influenced by extracellular concentrations, possibly importers ZIP1- ZIP8-mediated influx. The phosphorylation S6 kinase, substrate mTORC1, significantly enhanced inhibition PP2A, phosphatase contracting S6K consequently, increased activated These results new insight how modulate cytokines metabolic reprograming monocytes/macrophages.