title: Inhibition of proinflammatory activities of major periodontal pathogens by aqueous extracts from elder flower (Sambucus nigra).
abstract: BACKGROUND
  Prolonged induction of excessive levels of inflammatory mediators contributes to the pathogenesis of chronic disease states, such as periodontitis. It is thus important to develop safe and effective anti-inflammatory strategies for therapeutic reasons. In this study, we determined the ability of aqueous extracts from elder flower (Sambucus nigra) to inhibit the proinflammatory activity of major virulence factors from the periodontal pathogens Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans.
  
  
  METHODS
  Monocytes/macrophages or neutrophils were incubated with whole cells of P. gingivalis, A. actinomycetemcomitans, or purified components thereof (lipopolysaccharide and fimbriae) in the absence or presence of elder flower extract and were assayed for cytokine production, integrin activation, or induction of the oxidative burst.
  
  
  RESULTS
  The elder flower extract was found to potently inhibit all proinflammatory activities tested. Investigation of the underlying mechanisms revealed that the anti-inflammatory extract inhibited activation of the nuclear transcription factor kappaB and of phosphatidylinositol 3-kinase.
  
  
  CONCLUSIONS
  The elder flower extract displays useful anti-inflammatory properties that could be exploited therapeutically for the control of inflammation in human periodontitis.
authors.affiliation: Department of Pedodontics, School of Dentistry, Center of Excellence in Oral and Craniofacial Biology, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
authors.forename: Evlambia
authors.initials: E
authors.lastname: Harokopakis
authors.forename: Mohamad H
authors.initials: MH
authors.lastname: Albzreh
authors.forename: Elaine M
authors.initials: EM
authors.lastname: Haase
authors.forename: Frank A
authors.initials: FA
authors.lastname: Scannapieco
authors.forename: George
authors.initials: G
authors.lastname: Hajishengallis
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000187:drug effects* / Q000276:immunology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D039481:CD11b Antigen / Q000187:drug effects; D018821:CD18 Antigens / Q000187:drug effects; D010861:Fimbriae, Bacterial / Q000276:immunology; D035264:Flowers; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D007378:Interleukins / Q000037:antagonists & inhibitors; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D051379:Mice; D009000:Monocytes / Q000187:drug effects / Q000276:immunology; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010936:Plant Extracts / Q000494:pharmacology*; D016966:Porphyromonas gingivalis / Q000187:drug effects* / Q000276:immunology; D016897:Respiratory Burst / Q000187:drug effects; D027924:Sambucus nigra; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D037521:Virulence Factors / Q000037:antagonists & inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D039481:CD11b Antigen; D018821:CD18 Antigens; D018836:Inflammation Mediators; D007378:Interleukins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors