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

阐明唾液组蛋白与口腔细胞的存活和繁殖以及 Toll 样受体信号的相关性

基本信息

批准号：
18592051
负责人：
IMAMURA Yasuhiro
金额：
$ 2.55万
依托单位：
Matsumoto Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18592051/
关键词：
salivary protein histatin Toll-like receptor 熱ショックタンパク質相互作用

项目摘要

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.

环境因素被认为是牙周病的病因之一。它会破坏牙齿和软组织之间的粘连。牙槽骨的结缔组织和牵引组织也可被破坏。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。组胺素是一种与先天免疫系统相关的唾液蛋白，具有抗微生物、抑制变形链球菌生长和灭活牙周致病菌的胶原酶等作用。组胺素对宿主，特别是口腔细胞的作用目前还不清楚。我们研究了人牙龈成纤维细胞（HGF）和猪油中组胺素通过内吞作用进入热休克蛋白HSC 70。histatin/HSC 70复合物在生理条件下和热休克条件下分别轻微地和主题性地移位到裸细胞中。cellviability.in Toll样受体（Toll like receptors，TLRs）与先天免疫系统密切相关，TLRs的表达与细胞的免疫功能密切相关。几种HSP作为TLR的配体发挥作用。然而，尚未阐明HSC 70是否也成为配体。HSC 70刺激组成性表达TLR 4、CD 14和MD-2的293-TLRA/CD 14-MD-2细胞后，NF-κB被激活，而histatin/HSC 70复合物不作为配体，提示histatin阻断了HSC 70配体对TLR 4的作用。这意味着组胺素。是一种抗炎因子，通过NW-κB诱导阻止炎性细胞因子的产生。本研究结果为我们理解唾液蛋白组胺素在口腔内的先天免疫应答机制，进而发展为抗真菌、抗炎药物或生殖器官组织（细胞）提供了新的线索。