Login / Signup

Disruption of glucose homeostasis by bacterial infection orchestrates host innate immunity through NAD + /NADH balance.

Jingjing TangXiao WangShukun ChenTianyuan ChangYanchao GuFuhua ZhangJing HouYi LuoMengyuan LiJianan HuangMohua LiuLei ZhangYao WangXihui ShenLei Xu
Published in: Cell reports (2024)
Metabolic reprogramming is crucial for activating innate immunity in macrophages, and the accumulation of immunometabolites is essential for effective defense against infection. The NAD + /NADH (ratio of nicotinamide adenine dinucleotide and its reduced counterpart) redox couple serves as a critical node that integrates metabolic pathways and signaling events, but how this metabolite couple engages macrophage activation remains unclear. Here, we show that the NAD + /NADH ratio serves as a molecular signal that regulates proinflammatory responses and type I interferon (IFN) responses divergently. Salmonella Typhimurium infection leads to a decreased NAD + /NADH ratio by inducing the accumulation of NADH. Further investigation shows that an increased NAD + /NADH ratio correlates with attenuated proinflammatory responses and enhanced type I IFN responses. Conversely, a decreased NAD + /NADH ratio is linked to intensified proinflammatory responses and restrained type I IFN responses. These results show that the NAD + /NADH ratio is an essential cell-intrinsic factor that orchestrates innate immunity, which enhances our understanding of how metabolites fine-tune innate immunity.
Keyphrases
  • dendritic cells
  • escherichia coli
  • signaling pathway
  • ms ms
  • blood pressure
  • skeletal muscle
  • lymph node
  • cell therapy
  • mesenchymal stem cells
  • insulin resistance
  • listeria monocytogenes
  • glycemic control