title: Whole-blood cultures from patients with chronic periodontitis respond differently to Porphyromonas gingivalis but not Escherichia coli lipopolysaccharide.
abstract: BACKGROUND
  Porphyromonas gingivalis lipid A heterogeneity modulates cytokine expression in human cells. This study investigates the effects of two lipid A isoforms of P. gingivalis, lipopolysaccharide (LPS)1435/1449 and LPS1690, on the secretion of proinflammatory and regulatory cytokines in total blood cultures from patients with and without chronic periodontitis (CP).
  
  
  METHODS
  A cross-sectional study was conducted in 38 systemically healthy individuals divided in two groups: 1) the CP group (n = 19), in which patients were diagnosed with CP; and 2) the no periodontitis (NP) group (n = 19), which included control patients without CP. Blood samples were collected from all patients, and whole-blood cell cultures (WBCCs) were stimulated for 48 hours with P. gingivalis LPS1435/1449 and LPS1690 and Escherichia coli LPS. Unstimulated WBCCs served as negative controls. The secretion of interferon-γ (IFN-γ), interleukin-10 (IL-10), and transforming growth factor-β (TGF-β) was detected in WBCC supernatants by enzyme-linked immunosorbent assays.
  
  
  RESULTS
  E. coli LPS significantly increased the expression of all cytokines in WBCCs from both the NP and CP groups when compared to non-stimulated cells (control treatment). P. gingivalis LPS preparations increased IFN-γ levels in the CP group but not in the NP group when compared with controls (P <0.05). P. gingivalis LPS preparations also increased IL-10 and TGF-β levels in both CP and NP groups, but P. gingivalis LPS1690 showed a three-fold increase on IL-10 production in the NP group (P <0.05) when compared to P. gingivalis LPS1435/144.
  
  
  CONCLUSIONS
  These data demonstrate that WBCC cell populations obtained from healthy individuals and patients with CP may differ in the cytokine response to P. gingivalis but not E. coli LPS. This is consistent with the notion that CP alters the systemic WBCC response and that this can be detected by the different P. gingivalis LPS structures.
authors.affiliation: Department of Preventive Dentistry, University of Toronto, Toronto, ON.
authors.forename: Getulio
authors.initials: G
authors.lastname: Nogueira-Filho
authors.forename: Bruno Trevisan
authors.initials: BT
authors.lastname: Rosa
authors.forename: Patricia Ferreira
authors.initials: PF
authors.lastname: Santos
authors.forename: Urbino Rocha
authors.initials: UR
authors.lastname: Tunes
authors.forename: Songeli Menezes
authors.initials: SM
authors.lastname: Freire
authors.forename: Roberto
authors.initials: R
authors.lastname: Meyer
authors.forename: Richard P
authors.initials: RP
authors.lastname: Darveau
mesh_terms: D000328:Adult; D000368:Aged; D001773:Blood Cells / Q000187:drug effects; D055113:Chronic Periodontitis / Q000097:blood* / Q000145:classification; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood / Q000187:drug effects; D003774:Dental Plaque Index; D004926:Escherichia coli / Q000502:physiology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007371:Interferon-gamma / Q000097:blood / Q000187:drug effects; D016753:Interleukin-10 / Q000097:blood; D008050:Lipid A / Q000145:classification / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000097:blood / Q000145:classification; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000097:blood / Q000145:classification; D016966:Porphyromonas gingivalis / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000097:blood / Q000187:drug effects
chemical_list: D016207:Cytokines; C508609:IL10 protein, human; D018836:Inflammation Mediators; D008050:Lipid A; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D007371:Interferon-gamma