Effect of high glucose on the secretion of cytokines induced by Porphyromonas gingivalis lipopolysaccharide
10.3760/cma.j.issn.1002-0098.2014.12.009
- VernacularTitle:高糖对牙龈卟啉单胞菌脂多糖刺激人成纤维细胞分泌炎症因子的影响
- Author:
Shaoyun JIANG
1
;
Congcong WEI
;
Dong XUE
;
Jiayin DENG
;
Qi LIAN
;
Yunyun DONG
Author Information
1. 300070,天津医科大学口腔医院牙周科
- Keywords:
Porphyromonas gingivalis;
Lipopolysaccharides;
Periodontitis;
Tumor necrosis factor-α;
Interleukin-1 β
- From:
Chinese Journal of Stomatology
2014;49(12):737-741
- CountryChina
- Language:Chinese
-
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.
