Hydrogen sulfide synergistically upregulates Porphyromonas gingivalis lipopolysaccharide-induced expression of IL-6 and IL-8 via NF-κB signalling in periodontal fibroblasts

Hydrogen sulfide synergistically upregulates Porphyromonas gingivalis lipopolysaccharide-induced expression of IL-6 and IL-8 via NF-κB signalling in periodontal fibroblasts
复制标题

硫化氢通过牙周成纤维细胞中的 NF-κB 信号协同上调牙龈卟啉单胞菌脂多糖诱导的 IL-6 和 IL-8 表达。

DOI:
10.1016/j.archoralbio.2014.05.022
复制
发表时间:
2014-09-01
影响因子:
3
通讯作者:
Wang, Yi-Xiang
Wang, Yi-Xiang
中科院分区:
医学4区
文献类型:
--
作者:
Chi, Xiao-Pei;Ouyang, Xiang-Ying;Wang, Yi-Xiang

文献摘要

被引文献

相似文献

目的:牙周病原体牙龈卟啉单胞菌产生硫化氢(H_2S)。口腔中的H_2S与牙周炎呈正相关,但H_2S促进牙周病的机制尚不清楚。本实验观察了不同浓度的硫化氢供体NaHS对牙周成纤维细胞促炎细胞因子IL-6和IL-8表达的影响,并探讨其作用机制。用实时荧光定量聚合酶链式反应和酶联免疫吸附试验检测IL-6和IL-8的表达。结果:实时荧光定量聚合酶链式反应和酶联免疫吸附试验结果显示,硫化氢不仅以剂量和时间依赖的方式上调IL-6和IL-8在mRNA和蛋白水平的表达,而且还加重了牙龈假单胞菌内毒素诱导的GFS和PDLCs中IL-6和IL-8的表达。Western blotting和EMSA结果显示,NaHS、牙龈假单胞菌和脂多糖均可激活NF-kappa B信号转导通路,这与GFS和PDLCs中IL-6和IL-8的表达水平一致。结论:硫化氢通过激活NF-kappa B信号通路,协同上调牙龈假单胞菌诱导的GFS和PDLCs中IL-6和IL-8的表达,从而促进牙周炎的发生发展。(C)2014爱思唯尔有限公司。保留所有权利。
Objectives: The periodontal pathogen Porphyromonas gingivalis produces hydrogen sulfide (H2S). H2S in the oral cavity is positively correlated with periodontitis but the mechanism by which H2S contributes to periodontal diseases is obscure. We investigated the effect of H2S in combination with P. gingivalis lipopolysaccharide (LPS) on expression of the pro-inflammatory cytoldnes interleukin (IL)-6 and IL-8 in periodontal fibroblasts and the underlying mechanism of action.Material and methods: Gingival fibroblasts (GFs) and periodontal ligament cells (PDLCs) were treated with different concentrations of the H2S donor NaHS in the presence/absence of P. gingivalis LPS for different time periods. Expression of IL-6 and IL-8 was detected by real-time PCR and ELISA. The activity of nuclear factor-kappa B (NF-kappa B) signalling was investigated using western blotting, EMSA and pathway blockade assays.Results: Real-time PCR and ELISA results showed that H2S not only upregulated expression of IL-6 and IL-8 at mRNA and protein levels in a dose- and time-dependent manner, but also aggravated P. gingivalis LPS-induced expression of IL-6 and IL-8 in GFs and PDLCs. Western blotting and EMSA showed that NF-kappa B signalling was activated by NaHS, P. gingivalis LPS, and both, which was in accordance with the expression levels of IL-6 and IL-8 in GFs and PDLCs. These results were confirmed using a NF-kappa B pathway blockade assay.Conclusions: H2S synergistically upregulated P. gingivalis LPS-induced expression of IL-6 and IL-8 in GFs and PDLCs via activation of NF-kappa B signalling, which could promote the development of periodontitis. (C) 2014 Elsevier Ltd. All rights reserved.