title: Variable cell responses to P. gingivalis lipopolysaccharide.
abstract: Porphyromonas gingivalis is a major etiological agent of chronic periodontal diseases, the virulence of which has been attributed to different factors, including lipopolysaccharide (LPS). We investigated the differential responses induced by P. gingivalis LPS stimulation of human umbilical vein endothelial cells and human oral epithelial cells. RT-PCR analysis showed that P. gingivalis LPS used Toll-like receptor 2 (TLR2) to activate epithelial cells and Toll-like receptor 4 (TLR4) to activate endothelial cells. Both cell types were stimulated by P. gingivalis LPS to produce pro-inflammatory cytokines. Cytokine Array assay showed that although patterns of cytokine expression were similar in both cell types, some cytokines were specifically secreted by the endothelial cells, and others were specific to epithelial cells. These results support the idea that the same LPS preparation can act as a TLR2 or TLR4 agonist, depending on TLR expression of the host cell, inducing cytokine profiles that differ according to the cell type.
authors.affiliation: ERT-1061 internal to unit INSERM UMR-977, Dental Faculty, University of Strasbourg, 11 rue Humann, 67000 Strasbourg, France.
authors.forename: L
authors.initials: L
authors.lastname: Kocgozlu
authors.forename: R
authors.initials: R
authors.lastname: Elkaim
authors.forename: H
authors.initials: H
authors.lastname: Tenenbaum
authors.forename: S
authors.initials: S
authors.lastname: Werner
mesh_terms: D000911:Antibodies, Monoclonal; D002460:Cell Line; D002478:Cells, Cultured; D019742:Chemokines, CC / Q000032:analysis; D019743:Chemokines, CXC / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D042783:Endothelial Cells / Q000276:immunology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology*; D004847:Epithelial Cells / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007378:Interleukins / Q000032:analysis; D015603:Keratinocytes / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D009061:Mouth Mucosa / Q000166:cytology / Q000276:immunology*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D051195:Toll-Like Receptor 2 / Q000819:agonists / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000819:agonists / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014471:Umbilical Veins / Q000166:cytology / Q000276:immunology; D015854:Up-Regulation / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D019742:Chemokines, CC; D019743:Chemokines, CXC; D016207:Cytokines; D018836:Inflammation Mediators; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D007378:Interleukins; D008070:Lipopolysaccharides; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha