Activation of human gingival epithelial cells by black-pigmented bacteria

1. 人牙龈上皮细胞对普雷沃氏菌间质糖蛋白（PGP）和牙龈卟啉单胞菌的菌毛和脂多糖（LPS）部分产生白细胞介素(IL)-8、粒细胞集落刺激因子和粒细胞-巨噬细胞集落刺激因子。相反，在干扰素(IFN)- γ刺激下，细胞产生巨噬细胞集落刺激因子。2 .牙龈芽孢杆菌的PGP、菌毛和LPS组分增强了人牙龈上皮细胞表面细胞间黏附分子-1 （ICAM-1）的表达。通过逆转录酶pcr证实了黑色素细菌（black pigmentation bacteria， BPB）成分对细胞中上述细胞因子和ICAM-1的mRNA诱导作用。人类牙龈上皮细胞不表达主要的LPS受体CD14，这表明细胞被BPB成分激活的途径与肠杆菌科LPS不同。1998年，toll样受体（TLRs）被报道为UPS的信号分子，并且TLRs在高浓度LPS下以不依赖cd14的方式介导LPS信号。tlr通过BPB组分参与人牙龈上皮细胞活化的实验正在进行中。人牙龈上皮细胞具有IL-18，一种ifn - γ诱导因子，在细胞中可能作为前体形式存在。本研究使用的这些刺激剂均不能诱导细胞分泌IL-18。然而，有可能细胞产生的il -18通过某种刺激，如凋亡途径，诱导免疫细胞产生ifn - γ，进而产生ifn - γ参与牙周炎症的发生和治愈。

1. Human gingival epithelial cells produce interleukin (IL)-8, granulocyte-colony stimulating factor and granulocyte-macrophage colony stimulating factor in response to Prevotella intermedia glycoprotein (PGP), and fimbriae andl ipopolysaccharide (LPS) fraction of Porphyromonas gingivalis. In contrast, the cells produce macrophage-colony stimulating factor stimulated with interferon (IFN)-gamma.2. P.intermedia PGP, fimbriae and LPS fraction of P.gingivalis augmented the expression of intercellular adhesionmolecule-1 (ICAM-1) on the surface of human gingival epithelial cells, flow cytometically.3. mRNA induction of the above cytokines and ICAM-1 in the cells by the components of black-pigmented bacteria (BPB)was confirmed by reverse-transcriptase PCR.4. Human gingival epithelial cells do not express CD14, a major LPS receptor, which indicates that the cells are activated by the components of BPB with a distinct pathway from LPS of Enterobacteriaceae. In 1998, Toll-like receptors (TLRs)were reported to be signaling molecules of UPS, and also TLRs mediated LPS signal in a CD14-independent manner at a high concentration of LPS.The experiment that TLRs participate in the activation of human gingival epithelial cells by components of BPB is under way.5. Human gingivalepithelial cells possess IL-18, a IFN-gamma inducing factor, in the cells as a possibly precursor form. Thes timulants used in this study could not induce the secretion of IL-18 by the cells. However, it is possible that IL-18produced by the cells with some stimulation, such as apoptotic pathway may induce IFN-gamma by immune cells, and that in turn, IFN-gamma produced may participate in the onset and cure of inflammation in periodontium.