Bile acid receptor Tgr5 prevents macrophage hyperinflammation during bacterial sepsis through metabolic and epigenetic silencing

sepsis. Unexpectedly, Tgr5-deficient macrophages show reduced glycolysis and ATP citrate lyase expression, which cumulates in acetyl-CoA deficiency and impaired metabolic-epigenetic gene silencing, driving macrophages toward a hyperinflammatory phenotype during bacterial sepsis.