Activation of human gingival epithelial cells by black-pigmented bacteria

1.人牙龈上皮细胞对中间普氏菌糖蛋白（PGP）、牙龈卟啉单胞菌菌毛和脂多糖（LPS）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，细胞产生巨噬细胞集落刺激因子刺激干扰素（IFN）-γ。2.流式细胞术检测发现，中间型牙龈卟啉单胞菌PGP、菌毛和LPS组分均能促进人牙龈上皮细胞表面ICAM-1的表达.通过逆转录PCR证实了黑色素细菌（BPB）组分在细胞中对上述细胞因子和ICAM-1的mRNA诱导.人牙龈上皮细胞不表达CD 14，这是一种主要的LPS受体，这表明细胞被BPB的组分激活，具有与肠杆菌科LPS不同的途径。1998年，Toll样受体（Toll like receptors，TLRs）被报道为UPS的信号分子，并且在高浓度LPS下TLRs以非CD 14依赖的方式介导LPS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.人牙龈上皮细胞具有IL-18，IFN-γ诱导因子，在细胞中作为可能的前体形式。本研究中所用的刺激剂不能诱导细胞分泌IL-18。但是，牙周组织中细胞产生的IL-18可能通过某些刺激途径，如凋亡途径，诱导免疫细胞产生IFN-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.