The elucidation of salivary histatin, in correlation with survival and reproduction of oral cells, and Toll-like receptor signals

环境因素被认为是牙周病的病因学。它会破坏牙齿和软组织之间的粘连。而结缔组织和牵拉组织作为牙槽骨也可破坏。这种行为是由宿主细胞之间复杂的相互作用引起的慢性炎症。组蛋白是与天然免疫系统有关的唾液蛋白，具有抗C菌活性、抑制变形链球菌生长和灭活牙周病原体的胶原酶等作用。到目前为止，组抑素对宿主，特别是口腔细胞的作用尚不清楚。我们研究了组蛋白在人牙龈成纤维细胞(HGF)和热休克蛋白HSC70中的内吞作用。在生理和热休克条件下，组蛋白/HSC70复合体分别轻微和主题地移位到纽迪斯。在HGF中，Toll样受体(TLRs)与先天免疫系统有关。几个热休克蛋白作为TLR的配体发挥作用。然而，目前还不清楚HSC70是否也成为一种配体。2 93-TLRA/CD14-MD-2细胞TLR4、CD14和MD-2的组成性表达被HSC70刺激后，NF-κB被激活，而HSC70/HSC70复合体不再作为配体。提示组蛋白阻止了HSC70的TLR4配体的作用。这暗示了一种可能性，即组蛋白。是一种抗炎因子，通过NW-κB辐射阻止炎性细胞因子的产生。这一发现为我们理解口腔天然免疫反应的机制提供了新的线索，这些机制是通过研制抗真菌和抗炎药物或通过唾液蛋白组蛋白来繁殖组织(细胞)来实现的。

An environmental factor is mentioned as an etiology of periodontal diseases. It causes destruction of adhesion between teeth and soft tissue. And the connective and haul tissue hire as the alveolar bone can be also destruction. This behavior is induced chronic inflammation by the complicated interaction between host cells. Histatins are salivary proteins relative to innate immune system, which have an anti-C anima activity, growth inhibition of S.mutans and inactivation of collagenase from periodontal pathogens. The function of histatins against host, in particular oral cells, has not been understood sofar. We have studied that histatin is entned by endocytosis in human gingivalfibmblasts (HGF) and Lards to heat shockprotein HSC70. The histatin/HSC70 compiex is slightly and thematically traaslocated into nudeus at physiological and heat shocked conditions, respectively. And histatin is also enhanted both DNA synthesis and cellviability.in HGF.Toll-like receptors (TLRs) are relative to innate immune system. Several HSPs works as ligands against TLRs. However it has not been clarified whether HSC70 also becomes a ligand. When 293-TLRA/CD14-MD-2 cells, constitutive expression of TLR4, CD14 and MD-2, were stimulated with HSC70, NF-κB was activated Moreoveg histathr/HSC70 complex was not served as the ligand anylonget The resuk suggests that histatin prevents the role of ligand of HSC70 about TLR4. It implies the possibility that histatin. Is an anti-inflammatory factor preventing the production of inflammatory cytokines through the NW-κB adivation. The present findings provide new clues far our understanding of the mechanisms afinnate imaramoresponce in oral cavity folowedby development for antifimgal and anti-inflammatory drug or reproduction aforal tissues (cells) by salivary protein histatin.