title: Temporal induction of secretory leukocyte protease inhibitor (SLPI) in odontoblasts by lipopolysaccharide and wound infection.
abstract: BACKGROUND
  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.
authors: Department of Oral Histology, School of Dentistry, Chosun University, Dong-Gu, Gwangju, Korea.
authors: Baik-Dong
authors: BD
authors: Choi
authors: Soon-Jeong
authors: SJ
authors: Jeong
authors: Guanlin
authors: G
authors: Wang
authors: Heung-Joong
authors: HJ
authors: Kim
authors: Byung-Ock
authors: BO
authors: Kim
authors: Ho-Keel
authors: HK
authors: Hwang
authors: Do-Seun
authors: DS
authors: Lim
authors: Sook-Hyang
authors: SH
authors: Kim
authors: Moon-Jin
authors: MJ
authors: Jeong
mesh_terms: D000818:Animals; D002461:Cell Line, Transformed; D003782:Dental Pulp / Q000166:cytology / Q000378:metabolism*; D003804:Dentin / Q000378:metabolism; D004790:Enzyme Induction; D004926:Escherichia coli / Q000737:chemistry; D007150:Immunohistochemistry; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000494:pharmacology; D051379:Mice; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D009804:Odontoblasts / Q000378:metabolism*; D011671:Pulpitis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000096:biosynthesis* / Q000502:physiology; D015398:Signal Transduction; D013997:Time Factors; D014946:Wound Infection / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D053481:Secretory Leukocyte Peptidase Inhibitor; C506815:Slpi protein, mouse