title: Effect of IL-1ra on human dental pulp cells and pulpal inflammation.
abstract: OBJECTIVE
  This study was conducted to investigate the effect of interleukin-1 receptor antagonist (IL-1ra) on the LPS-induced interleukin-1beta (IL-1beta) synthesis in human dental pulp cells and to assess the role of IL-1ra in pulpal inflammation.
  
  
  METHODS
  IL-1beta from human dental pulp cells (HDP) was measured by sandwich ELISA; IL-1ra expression in pulpal tissue was detected by immunohistochemical staining.
  
  
  RESULTS
  Stimulation of HDP with increasing concentrations of FnLPS resulted in dose-dependent IL-1beta production. The addition of IL-1ra reduced FnLPS-induced IL-1beta synthesis in human dental pulp cells. Significant inhibition of the FnLPS-induced IL-1beta synthesis was observed when IL-1ra was added before treating with FnLPS for 60 min. Large numbers of IL-1ra positive neutrophils, plasmacytes, endothelial cells and lymphocytes were observed in inflamed pulp tissue.
  
  
  CONCLUSIONS
  IL-1ra could reduce LPS-stimulated IL-1beta synthesis, suggesting that IL-1ra may play a role in pulpitis.
authors.affiliation: Department of Endodontics, College of Stomatology, Fourth Military Medical University, Xi'an, China. luhuaix@netease.com
authors.forename: H-X
authors.initials: HX
authors.lastname: Lu
authors.forename: M-Z
authors.initials: MZ
authors.lastname: Xiao
authors.forename: Z-Y
authors.initials: ZY
authors.lastname: Niu
authors.forename: X-M
authors.initials: XM
authors.lastname: Guo
authors.forename: S-L
authors.initials: SL
authors.lastname: Zhao
authors.forename: H-G
authors.initials: HG
authors.lastname: Wang
authors.forename: H-Y
authors.initials: HY
authors.lastname: Guo
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D004396:Coloring Agents; D003782:Dental Pulp / Q000166:cytology / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D016967:Fusobacterium nucleatum; D006801:Humans; D007150:Immunohistochemistry; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis / Q000037:antagonists & inhibitors; D008070:Lipopolysaccharides / Q000494:pharmacology; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D010950:Plasma Cells / Q000187:drug effects / Q000473:pathology; D011671:Pulpitis / Q000473:pathology / Q000503:physiopathology*; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D011994:Recombinant Proteins; D012795:Sialoglycoproteins / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D004396:Coloring Agents; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D008070:Lipopolysaccharides; D017472:Receptors, Interleukin-1; D011994:Recombinant Proteins; D012795:Sialoglycoproteins