Dexamethasone Reduces Glycolysis and Inflammation in Human Macrophages Infected With Mycobacterium avium Without Compromising Bacterial Control.

Nontuberculous mycobacterial infections are associated with persistent inflammation and prolonged treatment, yet host-directed therapeutic strategies remain lacking. Using metabolic flux analysis, we show dexamethasone suppressed Mycobacterium avium-induced glycolysis in human monocyte-derived macrophages. Furthermore, dexamethasone reduced metabolic enzyme expression and proinflammatory cytokines, without affecting bacterial control in human macrophages. These findings indicate that suppression of glycolytic metabolism can occur without impacting bacterial control in human macrophages and supports further investigation of dexamethasone as a potential host-directed strategy to limit inflammation while preserving host defense in nontuberculous mycobacterial disease.