Resistance of LPS-activated bone marrow derived macrophages to apoptosis mediated by dexamethasone

摘要: Glucocorticoids (GC) display pleiotropic effects on the immune system. Macrophages are a major target for GC action. Here we show that dexamethasone (DEX), synthetic GC, decreased viability of naive bone marrow-derived macrophages (BMDM), involving an apoptotic mechanism. Administration DEX together with lipopolysaccharide (LPS) protected BMDM against DEX-mediated cell death, suggesting activated respond to differently than BMDM. An insight molecular basis LPS actions was provided by 7 fold increase in mRNA levels glucocorticoid receptor beta (GRβ), GR dominant-negative splice variant which inhibits GRα's transcriptional activity. did not inhibit all BMDM; significantly reduced percentage expressing high surface markers F4/80 and CD11b led decrease macrophage inflammatory protein 1 alpha (MIP1-α) levels. These two were prevented LPS. Our finding reduce DEX-induced elevation glucocorticoid-induced leucine zipper (GILZ), mediator GCs anti-inflammatory actions, may provide underlying findings enable better understanding clinical states, such as sepsis, endotoxins treatment is considered.