RESUMO
OBJECTIVE: In the present study, the role of macrophages and mast cells in mineral trioxide aggregate (MTA)-induced release of neutrophil chemotactic factor was investigated. STUDY DESIGN: MTA 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 muM/well), BWA4C (BW, 100 muM/well) or U75302 (U75, 10 muM/well). The concentration of Leukotriene B(4) (LTB(4)) in the cell-free supernatant from mast cells and macrophage culture was measured by ELISA. RESULTS: Supernatants 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)beta and macrophage inflammatory protein-2 (MIP-2) and the pretreatment of macrophages and mast cells with DEX, BW, or U75 significantly altered IL-1beta and MIP-2 mRNA expression. LTB(4) was detected in the MTA-stimulated macrophage supernatant but not mast cells. CONCLUSIONS: MTA-induces the release of neutrophil chemotactic factor substances from macrophages and mast cells with participation of IL-1beta, MIP-2, and LTB(4).
Assuntos
Compostos de Alumínio/farmacologia , Compostos de Cálcio/farmacologia , Citocinas/metabolismo , Leucotrieno B4/metabolismo , Macrófagos/efeitos dos fármacos , Mastócitos/efeitos dos fármacos , Óxidos/farmacologia , Materiais Restauradores do Canal Radicular/farmacologia , Silicatos/farmacologia , Compostos de Alumínio/imunologia , Análise de Variância , Animais , Compostos de Cálcio/imunologia , Ensaios de Migração de Leucócitos , Movimento Celular/efeitos dos fármacos , Movimento Celular/imunologia , Células Cultivadas , Quimiocina CXCL2/efeitos dos fármacos , Quimiocina CXCL2/genética , Quimiocina CXCL2/metabolismo , Meios de Cultivo Condicionados/farmacologia , Citocinas/efeitos dos fármacos , Citocinas/genética , Combinação de Medicamentos , Interleucina-1beta/efeitos dos fármacos , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-8/efeitos dos fármacos , Interleucina-8/genética , Interleucina-8/metabolismo , Leucotrieno B4/genética , Macrófagos/metabolismo , Masculino , Mastócitos/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Neutrófilos/efeitos dos fármacos , Neutrófilos/imunologia , Óxidos/imunologia , RNA Mensageiro/análise , Silicatos/imunologia , Estatísticas não ParamétricasRESUMO
INTRODUCTION: Mineral trioxide aggregate (MTA) and calcium silicate (CS) cements exhibit acceptable physical and chemical properties. The aim of the present study was to evaluate the effects of MTA and CS cements on inflammatory reactions in primary cultured human dental pulp cells. METHODS: The mitochondrial colorimetric assay was used to evaluate pulp cell survival rates. Fluorescent immunohistochemistry was used to observe focal adhesion kinase (FAK) and cyclooxygenase-2 (COX-2) distributions in the cells. Reverse transcription-polymerase chain reaction was used to assess COX-2 expression. RESULTS: The results showed that MTA and CS are biocompatible with pulp cells (P>.05). FAK was well-distributed in pulp cells in contact with both cements. Both MTA and CS cements induced pulp cell inflammation as evidenced by increased COX-2 expression. CONCLUSIONS: The present study demonstrated that MTA and CS cements are biocompatible with primary cultured pulp cells. Both cements can induce inflammatory COX-2 expression in the pulp cells.
