Temporal Induction of SLPI in Odontoblast by Infections and Wounds

Objective: 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 pro-inflammation signaling factors. From previous experiments, it was found that SLPI was expressed at low levels in mouse odontoblast-like cells (MDPC-23). Therefore, experiments were designed to identify the expression and function of SLPI in MDPC-23 and odontoblasts during the inflammatory response caused by infections and wounds. Methods: In this study, we used the RT-PCR, real-time RT-PCR, Western blotting with immunoprecipitation, scanning electron microscope (SEM) analysis, immuohistochemistry and measurement of luciferase activity for investigation of the SLPI expression and function in MDPC-23 cells by LPS and wound. The cavity was prepared in the first molar of maxillary on occlusal surface using the #330 conventional burs for induction of artificial wound. Results: The LPS treatment strongly increased the expression of SLPI mRNA at the initial stage. SLPI protein expression showed a time lag between translation and secretion. SLPI was expressed along the dentinal tubules and odontoblast layer in rat teeth after an artificial wound in immuohistochemistry. SLPI also inhibited the LPS-induced activation of NF-KappaB. This suggests that SLPI is a protease inhibitor in the absence of an infection but may participate in the anti-inflammatory response through NF-KappaB signaling in odontoblast-like cells. Conclusion: The odontoblast-like cells produce SLPI in response to LPS and wound stimulation in a manner similar to macrophages, and the secreted SLPI inhibits NF-KappaB activation. Therefore, the temporal induction of SLPI in odontoblast-like cells suggests that LPS up-regulates SLPI and SLPI antagonizes the LPS response, resulting in the inhibition of NF-KappaB activation and downstream gene expression. This work was supported by KRF (KRF-2006-311-E00171)& BK21. Correspondence should be addressed to Dr. Moon-Jin Jeong