Han Su-Ji, Jeong So-Yeon, Nam Yun-Ju, Yang Kyu-Ho, Lim Hoi-Soon, Chung Jin
Department of Oral Microbiology, School of Dentistry, Pusan National University, Pusan, Korea 602-739.
Clin Diagn Lab Immunol. 2005 Nov;12(11):1285-91. doi: 10.1128/CDLI.12.11.1285-1291.2005.
Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF-alpha and IL-1beta expression. The kinetics of TNF-alpha and IL-1beta levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF-alpha) and 2 to 4 h (IL-1beta), respectively. NF-kappaB, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF-kappaB activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF-kappaB). Pretreatment with xylitol inhibited LPS-induced TNF-alpha and IL-1beta gene expression and protein synthesis. LPS-induced mobilization of NF-kappaB was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.
牙龈卟啉单胞菌是可疑的牙周病致病菌之一。牙龈卟啉单胞菌的脂多糖(LPS)是牙周炎发生发展的关键因素。炎性细胞因子在以牙龈组织破坏为特征的牙周炎中起重要作用。巨噬细胞在慢性炎症部位较为突出,被认为与牙周炎的发病机制有关。木糖醇很突出,并且被广泛认为具有防龋特性。然而,迄今为止,关于木糖醇对牙周炎的影响知之甚少。本研究的目的是确定用牙龈卟啉单胞菌LPS刺激RAW 264.7细胞时肿瘤坏死因子α(TNF-α)和白细胞介素-1β(IL-1β)的表达情况,以及木糖醇对LPS诱导的TNF-α和IL-1β表达的影响。LPS处理后培养上清液中TNF-α和IL-1β水平的动力学显示,分别在1小时(TNF-α)和2至4小时(IL-1β)达到峰值。转录因子核因子κB(NF-κB)也被LPS处理激活。这些细胞因子表达和NF-κB激活被吡咯烷二硫代氨基甲酸盐(NF-κB抑制剂)预处理所抑制。木糖醇预处理可抑制LPS诱导的TNF-α和IL-1β基因表达及蛋白质合成。木糖醇预处理还以剂量依赖的方式抑制LPS诱导的NF-κB激活。木糖醇对牙龈卟啉单胞菌的生长也有抑制作用。综上所述,这些发现表明木糖醇可能不仅因其对LPS诱导的炎性细胞因子表达的抑制作用而对龋齿有良好临床效果,对牙周炎也有良好临床效果。