Activation of human gingival epithelial cells by black-pigmented bacteria

1.人牙龈上皮细胞产生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，作用于中间普氏杆菌糖蛋白(PGP)和牙龈卟啉单胞菌菌毛和脂多糖(LPS)部分。相反，细胞在干扰素-γ刺激下产生巨噬细胞集落刺激因子。中间假单胞菌PGP、菌毛和牙龈假单胞菌脂多糖组分可促进人牙龈上皮细胞表面细胞间黏附分子-1(ICAM-1)的表达，并呈胞浆状分布。逆转录-聚合酶链式反应(RT-RT)证实黑色素细菌(BPB)组分对上述细胞因子和ICAM-1的mRNA诱导作用。人牙龈上皮细胞不表达主要的内毒素受体CD14，这表明该细胞被BPB的成分激活，具有与肠杆菌科细菌脂多糖不同的途径。1998年，Toll样受体(Toll-like Receptor，TLRs)被报道为UPS的信号分子，在高浓度LPS中，TLRs也以CD14非依赖的方式介导内毒素信号。TLRs参与BPB组分激活人牙龈上皮细胞的实验正在进行中。人牙龈上皮细胞中含有IL-18，这是一种干扰素-γ诱导因子，可能是其前体。本研究中使用的刺激剂不能诱导细胞分泌IL-18。然而，细胞在某些刺激条件下产生的IL-18可能通过免疫细胞诱导产生干扰素-γ，进而参与牙周组织炎症的发生和治疗。

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.