title: Porphyromonas gingivalis-induced inflammatory mediator profile in an ex vivo human whole blood model.
abstract: Periodontitis is characterized by an accumulation of inflammatory cells in periodontal tissue and subgingival sites. Leukocytes play a major role in the host response to Porphyromonas gingivalis, a major aetiological agent of chronic periodontitis. Secretion of high levels of inflammatory mediators, including cytokines and prostaglandins, by leucocytes is believed to contribute to periodontal tissue destruction. The aim of this study was to investigate the inflammatory response of an ex vivo whole blood model to P. gingivalis stimulation. The production of interleukin-1 beta (IL-1beta), IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), IFN-gamma-inducible protein 10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), Regulated on Activation Normal T cell Expressed and Secreted (RANTES) and prostaglandin E2 (PGE2) were quantified by enzyme-linked immunosorbent assays. P. gingivalis induced the secretion of the pro-inflammatory cytokines IL-1beta, TNF-alpha, IL-6 and IFN-gamma, the chemokines IL-8, RANTES and MCP-1 and the inflammatory mediator PGE2 in an ex vivo human whole blood model. The secretion levels were dependent on the strain and the infectious dose used. While the mediator profiles were comparable between six healthy subjects, a high interindividual variability in the levels of secreted mediators was observed. This study supports the view that P. gingivalis, by inducing high levels of inflammatory mediators from a mixed leucocyte population, can contribute to the progression of periodontitis.
authors.affiliation: Groupe de Recherche en Ecologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, Quebec, Canada.
authors.forename: C
authors.initials: C
authors.lastname: Bodet
authors.forename: F
authors.initials: F
authors.lastname: Chandad
authors.forename: D
authors.initials: D
authors.lastname: Grenier
mesh_terms: D000704:Analysis of Variance; D001431:Bacteriological Techniques / Q000379:methods; D016866:Bacteroidaceae Infections / Q000276:immunology*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D015232:Dinoprostone / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D010518:Periodontitis / Q000276:immunology*; D016966:Porphyromonas gingivalis / Q000378:metabolism / Q000502:physiology*; D012709:Serum Albumin / Q000378:metabolism; D013045:Species Specificity; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D012709:Serum Albumin; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D015232:Dinoprostone