title: [Effect of high glucose on the secretion of cytokines induced by Porphyromonas gingivalis lipopolysaccharide].
abstract: OBJECTIVE
  To investigate the influence of high glucose on Porphyromonasgingivalis (Pg) lipopolysaccharide (LPS) stimulating human gingival fibroblasts (HGF) to secret the cytokines.
  
  
  METHODS
  HGF were obtained from the primary culture of the tissue explants. Cells were divided into four groups, low glucose (5.5 mmol/L) + 1 mg/L Pg LPS (group A);low glucose + 10 mg/L Pg LPS (group B); high glucose (25 mmol/L) +1 mg/L Pg LPS(group C); high glucose+10 mg/L Pg LPS (group D). The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cell supernatants were detected by enzyme- linked immunosorbent assay at 6 h and 12 h. The expressions of toll-like receptor 2, 4 (TLR-2, 4) were examined by real-time polymerase chain reaction. After pretreatment with anti-TLR2 and anti-TLR4 monoclonal antibody in HGF, TNF-α and L-1β levels were detected.
  
  
  RESULTS
  TNF-α concentration increased obviously in high glucose 6 h and 12 h after Pg LPS stimulation (P < 0.01). IL-1β secretion increased (P < 0.01). Meanwhile, TLR2, 4 mRNA expression increased, especially in high glucose+10 mg/L Pg LPS (P < 0.01). After inhibition of the TLR2, 4 in high glucose + 10 mg/L Pg LPS respectively, TNF-α level [(297.16±11.49), (390.01±12.81) ng/L] decreased (F = 166.02, P < 0.01), and IL-1β level [(49.90±4.08), (99.35±5.01) ng/L] also decreased (F = 153.51, P < 0.01).
  
  
  CONCLUSIONS
  High glucose may promote Pg LPS to stimulate the secretion of TNF-α and IL-1β through regulating TLR2, 4 expression, which suggests that the elevating blood glucose precipitate in aggravating the process of periodontal disease.
authors.affiliation: Department of Periodontics, Hospital of Stomatology, Tianjin Medical University, Tianjin 300070, China. Email: jiangshaoyun11@126.com.
authors.forename: Shaoyun
authors.initials: S
authors.lastname: Jiang
authors.forename: Congcong
authors.initials: C
authors.lastname: Wei
authors.forename: Dong
authors.initials: D
authors.lastname: Xue
authors.forename: Jiayin
authors.initials: J
authors.lastname: Deng
authors.forename: Qi
authors.initials: Q
authors.lastname: Lian
authors.forename: Yunyun
authors.initials: Y
authors.lastname: Dong
mesh_terms: D000911:Antibodies, Monoclonal; D004357:Drug Synergism; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism*; D010510:Periodontal Diseases / Q000209:etiology; D011135:Polysaccharides, Bacterial / Q000633:toxicity*; D016966:Porphyromonas gingivalis / Q000737:chemistry*; D013997:Time Factors; D051195:Toll-Like Receptor 2 / Q000276:immunology / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000276:immunology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D000911:Antibodies, Monoclonal; D053583:Interleukin-1beta; D011135:Polysaccharides, Bacterial; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose