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Objectives:  To investigate the effect of dexamethasone on triggering receptor expressed on myeloid cells-1 (TREM-1).   Methods:  Wild-type and tumor necrosis factor ( TNF  −/− ) mice were pre-treated with saline, dexamethasone, or hydrocortisone and exposed to a lethal infection of  Pseudomonas aeruginosa . Mortality and TREM-1 on neutrophil membranes was measured after sacrifice. U937 human monocytic cells were stimulated with lipopolysaccharide (LPS) or heat-killed  P. aeruginosa  without or with dexamethasone or hydrocortisone, and cell-surface TREM-1 and soluble TREM-1 (sTREM-1) were quantified. Expression of TREM-1 and sTREM-1 was also studied in LPS-stimulated U937 cells incubated in the absence or presence of TNFα or anti-TNFα antibody.   Results:  Pre-treatment with dexamethasone, but not hydrocortisone, prolonged animal survival. Mice pre-treated with dexamethasone showed decreased expression of TREM-1 on neutrophils. In U937 cells, LPS or heat-killed  P. aeruginosa  induced the expression of TREM-1 and the release of sTREM-1. U937 TREM-1 and sTREM-1 were decreased upon addition of dexamethasone but not hydrocortisone. The suppressive effect of dexamethasone was enhanced in the presence of exogenous TNFα and lost in the presence of anti-TNFα antibody. In  TNF  −/−  mice, dexamethasone suppression of mortality and TREM-1 neutrophil expression was lost. Gene expression of  TREM-1  in U937 monocytes was decreased after treatment with dexamethasone.   Conclusion:  TREM-1/sTREM-1 is a novel site of action of dexamethasone. This action is associated with down-regulation of gene expression and is mediated by TNFα.

Dexamethasone Down-Regulates Expression of Triggering Receptor Expressed on Myeloid Cells-1: Evidence for a TNFα-Related Effect