INTRODUCTION: The secretory leukocyte protease inhibitor (SLPI) is a bacterial lipopolysaccharide (LPS)-induced product of macrophages that antagonizes the LPS-induced activation of a number of proinflammatory signaling factors. From our previous experiments, it was found that SLPI was expressed slightly in odontoblast-like cells (MDPC-23). Therefore, these experiments were designed to determine the function of SLPI in MDPC-23 and odontoblasts during the inflammatory response caused by infections and wounds. METHODS: MDPC-23 cells were exposed to 100 ng/mL Escherichia coli LPS, and artificial wounds were induced in the right first molar of the maxillary of rats. In addition, a morphological change in the MDPC-23 cells was observed after LPS treatment. MDPC-23 cells were transfected transiently with the nuclear factor kappa-B (NF-kappaB) promoter binding vector. RESULTS: The level of SLPI expression increased strongly 30 minutes after the LPS treatment. Scanning electron microscopy revealed many extensions of the cytoplasmic processes after LPS stimulation. SLPI was expressed along the dentinal tubules and odontoblasts layer in rat teeth after an artificial wound. SLPI also inhibited the LPS-induced activation of NF-kappaB in MDPC-23. CONCLUSIONS: We report for the first time that SLPI is expressed temporally in infected odontoblasts and may participate in the anti-inflammatory response through NF-kappaB signaling in odontoblast-like cells.
INTRODUCTION: The secretory leukocyte protease inhibitor (SLPI) is a bacterial lipopolysaccharide (LPS)-induced product of macrophages that antagonizes the LPS-induced activation of a number of proinflammatory signaling factors. From our previous experiments, it was found that SLPI was expressed slightly in odontoblast-like cells (MDPC-23). Therefore, these experiments were designed to determine the function of SLPI in MDPC-23 and odontoblasts during the inflammatory response caused by infections and wounds. METHODS: MDPC-23 cells were exposed to 100 ng/mL Escherichia coli LPS, and artificial wounds were induced in the right first molar of the maxillary of rats. In addition, a morphological change in the MDPC-23 cells was observed after LPS treatment. MDPC-23 cells were transfected transiently with the nuclear factor kappa-B (NF-kappaB) promoter binding vector. RESULTS: The level of SLPI expression increased strongly 30 minutes after the LPS treatment. Scanning electron microscopy revealed many extensions of the cytoplasmic processes after LPS stimulation. SLPI was expressed along the dentinal tubules and odontoblasts layer in rat teeth after an artificial wound. SLPI also inhibited the LPS-induced activation of NF-kappaB in MDPC-23. CONCLUSIONS: We report for the first time that SLPI is expressed temporally in infected odontoblasts and may participate in the anti-inflammatory response through NF-kappaB signaling in odontoblast-like cells.