title: Porphorymonas gingivalis induces intracellular adhesion molecule-1 expression in endothelial cells through the nuclear factor-kappaB pathway, but not through the p38 MAPK pathway.
abstract: OBJECTIVE
  Porphyromonas gingivalis is a major pathogen in the development and progression of periodontal disease. The aim of this study was to investigate whether endothelial intracellular adhesion molecule-1 (ICAM-1), an inflammation biomarker for periodontitis, could be modified by infection with either of two strains of P. gingivalis with different virulence capacities: avirulent ATCC 33277 and virulent W83.
  
  
  METHODS
  We examined the expression of ICAM-1, IκBα, phospho-p38 MAPK and nuclear factor-kappaB (NF-κB) p65 in an umbilical vein endothelial cell line (ECV-304) treated with ATCC 33277 and W83, with or without the NF-κB antagonist MG132 and/or a specific p38 inhibitor (SB203580), by real-time PCR, western blotting and immunofluorescence.
  
  
  RESULTS
  Both strains could induce ICAM-1 expression; additionally W83 was able to increase ICAM-1 expression more significantly than ATCC 33277. In P. gingivalis-infected endothelial cells, both p38 MAPK and NF-κB signaling pathways were triggered by a rapid increase of p38 MAPK phosphorylation and a more delayed degradation of IκBα, followed by the nuclear translocation of NF-κB. It was found that ICAM-1 production in endothelial cells was abrogated by inhibition of the NF-κB pathway, but not by inhibition of the p38 MAPK pathway, using the inhibitors of the latter two molecules.
  
  
  CONCLUSIONS
  The induction of ICAM-1 by infection of umbilical vein endothelial cells with P. gingivalis might be mediated through the NF-κB pathway, but not by the p38 MAPK pathway.
authors.affiliation: Department of Periodontics, School of Stomatology, China Medical University, Shenyang, Liaoning Province, China.
authors.forename: D
authors.initials: D
authors.lastname: Zhang
authors.forename: H
authors.initials: H
authors.lastname: Zheng
authors.forename: J
authors.initials: J
authors.lastname: Zhao
authors.forename: L
authors.initials: L
authors.lastname: Lin
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Pan
mesh_terms: D021581:Active Transport, Cell Nucleus; D000704:Analysis of Variance; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism / Q000382:microbiology*; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000235:genetics; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010518:Periodontitis / Q000378:metabolism / Q000382:microbiology*; D010766:Phosphorylation; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction; D013045:Species Specificity; D051996:Transcription Factor RelA / Q000096:biosynthesis; D014471:Umbilical Veins / Q000166:cytology; D037521:Virulence Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D051996:Transcription Factor RelA; D037521:Virulence Factors; D018799:Intercellular Adhesion Molecule-1; D000072000:NF-KappaB Inhibitor alpha; D048051:p38 Mitogen-Activated Protein Kinases