title: Differential cytokine patterns in mouse macrophages and gingival fibroblasts after stimulation with porphyromonas gingivalis or Escherichia coli lipopolysaccharide.
abstract: BACKGROUND
  A major cause of chronic inflammatory periodontal disease is Porphyromonas gingivalis, a non-motile, Gram-negative, rod-shaped, anaerobic bacterium. Within gingival tissue, both macrophages and fibroblasts participate in the immune response to foreign entities by releasing cytokines and expressing molecules to recruit and activate lymphocytes. However, the contribution of gingival macrophages and fibroblasts to the immune response to P. gingivalis infection is not fully known.
  
  
  METHODS
  The AMJ2-C8 cell line (AM cells), a mouse alveolar macrophage cell line, and ESK-1 cells, a mouse gingival fibroblast cell line made in our laboratory, were treated with lipopolysaccharide (LPS) from either P. gingivalis or Escherichia coli. The expression of immune response molecules was quantified by real-time polymerase chain reaction and enzyme-linked immunoassay.
  
  
  RESULTS
  AM and ESK-1 cells responded differently to P. gingivalis and E. coli LPS stimulation. The ESK-1 gingival fibroblast cell line was more responsive to E. coli LPS stimulation as seen by elevated levels of interleukin (IL)-6, inducible nitric oxide, and monocyte chemotactic protein-1 expression relative to stimulation by P. gingivalis LPS. Conversely, the AM macrophage cell line was more responsive to P. gingivalis LPS stimulation, particularly for interleukin IL-1β, IL-6, and monocyte chemotactic protein-1, relative to stimulation by E. coli LPS.
  
  
  CONCLUSIONS
  These findings demonstrate that E. coli LPS induces a stronger cytokine and chemokine response in gingival fibroblasts, whereas P. gingivalis LPS induces a stronger response in macrophages.
authors.affiliation: Department of Diagnostic Sciences, Dental Branch, University of Texas Health Science Center at Houston, Houston, TX 77054, USA.
authors.forename: Katy J
authors.initials: KJ
authors.lastname: Jones
authors.forename: Sanaz
authors.initials: S
authors.lastname: Ekhlassi
authors.forename: Dina
authors.initials: D
authors.lastname: Montufar-Solis
authors.forename: John R
authors.initials: JR
authors.lastname: Klein
authors.forename: Jeremy S
authors.initials: JS
authors.lastname: Schaefer
mesh_terms: D000818:Animals; D002461:Cell Line, Transformed; D018932:Chemokine CCL2 / Q000032:analysis / Q000276:immunology; D054405:Chemokine CCL3 / Q000032:analysis / Q000276:immunology; D054407:Chemokine CCL4 / Q000032:analysis / Q000276:immunology; D016207:Cytokines / Q000032:analysis / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D004926:Escherichia coli / Q000276:immunology*; D005260:Female; D005347:Fibroblasts / Q000276:immunology* / Q000382:microbiology; D005881:Gingiva / Q000166:cytology / Q000276:immunology* / Q000382:microbiology; D053583:Interleukin-1beta / Q000032:analysis / Q000276:immunology; D053759:Interleukin-23 / Q000032:analysis / Q000276:immunology; D015850:Interleukin-6 / Q000032:analysis; D008070:Lipopolysaccharides / Q000276:immunology*; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D052247:Nitric Oxide Synthase Type II / Q000032:analysis / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C491768:Ccl2 protein, mouse; C496535:Ccl4 protein, mouse; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D016207:Cytokines; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; D008070:Lipopolysaccharides; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse