Mineral trioxide aggregate stimulates macrophages and mast cells to release neutrophil chemotactic factors: role of IL-1β, MIP-2 and LTB4

ObjectiveIn the present study, the role of macrophages and mast cells in mineral trioxide aggregate (MTA)-induced release of neutrophil chemotactic factor was investigated.Study designMTA suspension (50 mg/mL) was plated over inserts on macrophages or mast cells for 90 minutes. Untreated cells served as controls. Cells were washed and cultured for 90 minutes in RPMI without the stimuli. Macrophages and mast cell supernatants were injected intraperitoneally (0.5 mL/cavity), and neutrophil migration was assessed 6 hours later. In some experiments, cells were incubated for 30 minutes with dexamethasone (DEX, 10 μM/well), BWA4C (BW, 100 μM/well) or U75302 (U75, 10 μM/well). The concentration of Leukotriene B4 (LTB4) in the cell-free supernatant from mast cells and macrophage culture was measured by ELISA.ResultsSupernatants from MTA-stimulated macrophages and mast cells caused neutrophil migration. The release of neutrophil chemotactic factor by macrophages and mast cells was significantly inhibited by DEX, BW, or U75. Macrophages and mast cells expressed mRNA for interleukin-1 (IL-1)β and macrophage inflammatory protein-2 (MIP-2) and the pretreatment of macrophages and mast cells with DEX, BW, or U75 significantly altered IL-1β and MIP-2 mRNA expression. LTB4 was detected in the MTA-stimulated macrophage supernatant but not mast cells.ConclusionsMTA-induces the release of neutrophil chemotactic factor substances from macrophages and mast cells with participation of IL-1β, MIP-2, and LTB4.