Innate immune system in oral mucosa, with special reference to inhibition of inflammatory and immune responses and up-regulation of antibacterial functions
口腔粘膜的先天免疫系统,特别是抑制炎症和免疫反应以及上调抗菌功能
基本信息
- 批准号:18390484
- 负责人:
- 金额:$ 11.28万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 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:
- 关键词:
项目摘要
In the innate immune system, common and peculiar structures of microbes, pathogen-associated molecular patterns (PAMPs), are recognized by pattern-recognition molecules (PRMs) such as Toll-like receptors (TLRs) and NOD1/2 in host cells. We examined the innate immune system in the oral and related mucosa and obtained the following findings. 1) Oral and various epithelial cells (total of 16 lining cells) expressed TLR2 and 4 on the cell-surface and TLR3, 7, NOD1 and NOD2 intracellularly. The epithelial cells in general did not secrete inflammatory cytokines upon stimulation with respective synthetic ligands, whereas the cells actively produced antimicrobial factors such as peptidoglycan recognition proteins (PGRP-L, Iα, Iβ, S) and β-defensin 2. These findings suggest that epithelial cells, which interact with various microbes in normal flora, are negatively controlled to prevent the induction of excessive inflammatory and immune responses, while they actively produce anti-microbial factors. 2) Combined stimulation with TLR and NOD1/2 ligands synergistically induced anti-microbial factors in oral epithelial cells. 3) Minimal NOD1 ligand has been reported to be iE-DAP [γ-D-glutamy1-meso-diaminopimelic acid (γ-D-Glu-meso-DAP)]. We demonstrated that meso-DAP and meso-lanthionine by themselves activated various human epithelial cells via NOD1. When the resistant cells were treated to increase their permeability, meso-DAP clearly activated the cells, suggesting that meso-DAP is sufficient to activate NOD1 and that the D-Glu portion is required for the NOD-ligand to be incorporated into cells. 4) On the other hand, human gingival fibroblasts, which are isolated from normal flora, expressed TLR1-9 and NOD1/2, and actively produce inflammatory cytokines upon stimulation with the respective synthetic ligands.
在先天免疫系统中,微生物的常见和特殊结构,病原体相关分子模式(PAMP),被宿主细胞中的模式识别分子(PRM)如Toll样受体(TLR)和NOD 1/2识别。我们检查了口腔和相关粘膜中的先天免疫系统,并获得了以下发现。1)口腔和各种上皮细胞(总共16个衬里细胞)在细胞表面表达TLR 2和4,在细胞内表达TLR 3、7、NOD 1和NOD 2。上皮细胞在用相应的合成配体刺激时通常不分泌炎性细胞因子,而细胞主动产生抗微生物因子,如肽聚糖识别蛋白(PGRP-L、Iα、Iβ、S)和β-防御素2。这些发现表明,与正常植物群中的各种微生物相互作用的上皮细胞受到负控制,以防止诱导过度的炎症和免疫反应,同时它们积极产生抗微生物因子。2)TLR和NOD 1/2配体的联合刺激协同诱导口腔上皮细胞中的抗微生物因子。3)据报道,最小NOD 1配体是iE-DAP [γ-D-谷氨酰-内消旋-二氨基庚二酸(γ-D-Glu-内消旋-DAP)]。我们证明了meso-DAP和meso-lanthiblide本身通过NOD 1激活各种人上皮细胞。当抗性细胞被处理以增加其渗透性时,meso-DAP清楚地激活了细胞,这表明meso-DAP足以激活NOD 1,并且D-Glu部分是NOD-配体掺入细胞所需的。4)另一方面,从正常植物群分离的人牙龈成纤维细胞表达TLR 1 -9和NOD 1/2,并且在用相应的合成配体刺激时活跃地产生炎性细胞因子。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Toll-like receptors, NOD1, and NOD2 in oral epithelial cells
- DOI:10.1177/154405910608500609
- 发表时间:2006-06-01
- 期刊:
- 影响因子:7.6
- 作者:Sugawara, Y.;Uehara, A.;Takada, H.
- 通讯作者:Takada, H.
Meso-diaminopimelic acid and meso-lanthionine, amino acids peculiar to bacterial cell-wall peptidoglycans, activate human epithelial cells in culture via NOD1
内消旋二氨基庚二酸和内消旋羊毛硫氨酸是细菌细胞壁肽聚糖特有的氨基酸,通过 NOD1 激活培养物中的人上皮细胞
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:Uehara;A.
- 通讯作者:A.
Antibodies to proteinase 3 prime human monocytic cells via protease-activated receptor-2 and NF-κB for Toll-like recepor- andNOD-dependent activation.
蛋白酶 3 抗体通过蛋白酶激活受体 2 和 NF-κB 启动人类单核细胞,实现 Toll 样受体和 NOD 依赖性激活。
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:Uehara;A.;A. Iwashiro;T. Sato;S. Yokota;and H. Takada.
- 通讯作者:and H. Takada.
Antibodies to proteinase 3 prime human monocytic cells via protease-activatedpreceptor-2, phospholipase C, and NF-_kB for CD14-, Toll-like receptor 2-, 3-, 4-, 7-, 8-, N0D1-, and 2-dependent activation
蛋白酶 3 抗体通过蛋白酶激活的受体 2、磷脂酶 C 和 NF-_kB 介导 CD14-、Toll 样受体 2-、3-、4-、7-、8-、N0D1- 和 2
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Uehara. A.;and H. Takada
- 通讯作者:and H. Takada
Antibodies to proteinase 3 (PR3) prime human monocytic cells in a protease-activated receptor (PAR)-2-, proteinase 3-, phospholipase C-, and NF-k_B-dependent manner for CD14-, Toll-like receptor (TLR)2-, 3-, 4-, 7-, 8-, NOD1-, and 2-mediated activation
蛋白酶 3 (PR3) 抗体以蛋白酶激活受体 (PAR)-2-、蛋白酶 3-、磷脂酶 C- 和 NF-k_B 依赖性方式启动人单核细胞 CD14-、Toll 样受体 (TLR)
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Uehara. A.;and H. Takada.
- 通讯作者:and H. Takada.
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TAKADA Haruhiko其他文献
TAKADA Haruhiko的其他文献
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{{ truncateString('TAKADA Haruhiko', 18)}}的其他基金
Commensalism with oral streotococci: Up-regulation of innate immunity
与口腔链球菌共生:先天免疫的上调
- 批准号:
25670794 - 财政年份:2013
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Innate Immune Response via Intracellular Receptor NODs and Periodontal Diseases
通过细胞内受体 NOD 的先天免疫反应和牙周病
- 批准号:
16390519 - 财政年份:2004
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Periodontal Diseases as a Hypersensitivity Reaction Based on Innate Immune Responses in Periodontal Tissues
牙周病是一种基于牙周组织先天免疫反应的超敏反应
- 批准号:
14370576 - 财政年份:2002
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Recognition of Cell-Surface Components of Bacteria in Innate Immune System, with Special Reference to the Role of Toll-Like Receptors
先天免疫系统中细菌细胞表面成分的识别,特别是 Toll 样受体的作用
- 批准号:
12470380 - 财政年份:2000
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Bacterial cell surface amphiphiles and periodontal diseases - Study on the role of CD14 molecule in periodontal tissues -
细菌细胞表面两亲物与牙周疾病-CD14分子在牙周组织中的作用研究-
- 批准号:
10470378 - 财政年份:1998
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Superantigen Produced by oral Streptococci and oral mucosal diseases.
超抗原由口腔链球菌和口腔粘膜疾病产生。
- 批准号:
08457483 - 财政年份:1996
- 资助金额:
$ 11.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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