title: P. gingivalis and E. coli lipopolysaccharides exhibit different systemic but similar local induction of inflammatory markers.
abstract: BACKGROUND
  Porphyromonas gingivalis is a Gram-negative bacterium that is an important etiologic agent of human adult periodontitis. The goal of the study was to test the hypothesis that two isoforms of P. gingivalis lipopolysaccharide (PgLPS), PgLPS(1435)(/1449) and PgLPS(1690), exhibit differences in their capacity to stimulate systemic versus local responses compared to Escherichia coli lipopolysaccharide (LPS).
  
  
  METHODS
  LPS was inoculated into the scalp of mice, and the response was measured locally at the site of inoculation and systemically in the heart/aorta. Vascular cell adhesion molecule (VCAM)-1 was assessed at the protein level by enzyme-linked immunosorbent assay, and VCAM-1, E-selectin, and intercellular adhesion molecule (ICAM)-1 were assessed at the RNA level of the RNase protection assay. Serum tumor necrosis factor-alpha (TNF-alpha) levels were also measured.
  
  
  RESULTS
  E. coli LPS and both isoforms of P. gingivalis LPS were relatively potent in stimulating the expression of inflammatory markers, with E. coli LPS being more potent. In contrast, when the systemic response was measured in the heart/aorta, E. coli LPS, but not P. gingivalis LPS, significantly induced inflammatory markers. At moderate to low doses (1 and 10 microg per injection), serum TNF-alpha levels were minimally induced by P. gingivalis LPS compared to E. coli LPS.
  
  
  CONCLUSIONS
  Both forms of P. gingivalis LPS stimulated an inflammatory response when injected into connective tissue but were minimally stimulatory when a systemic response was measured. In contrast, E. coli LPS was a potent stimulus at the systemic and local levels.
authors.affiliation: Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA.
authors.forename: Rongkun
authors.initials: R
authors.lastname: Liu
authors.forename: Tesfahun
authors.initials: T
authors.lastname: Desta
authors.forename: Markos
authors.initials: M
authors.lastname: Raptis
authors.forename: Richard P
authors.initials: RP
authors.lastname: Darveau
authors.forename: Dana T
authors.initials: DT
authors.lastname: Graves
mesh_terms: D000818:Animals; D001011:Aorta / Q000276:immunology; D003238:Connective Tissue / Q000276:immunology; D004195:Disease Models, Animal; D019040:E-Selectin / Q000032:analysis; D004926:Escherichia coli / Q000276:immunology*; D018836:Inflammation Mediators / Q000032:analysis / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008070:Lipopolysaccharides / Q000145:classification / Q000276:immunology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009206:Myocardium / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D012535:Scalp / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D019040:E-Selectin; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1