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PGE_2 production in macrophages and bone resorption by etiologic agents of human periodontal diseases

巨噬细胞中 PGE_2 的产生和人类牙周病病因引起的骨吸收

基本信息

批准号：
08457496
负责人：
SAKAMOTO Wataru
金额：
$ 3.71万
依托单位：
HOKKIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08457496/
关键词：
Porphyromonas ginigivalis Periodontal disease Macrophage PGE_2 IL-1beta TNF- alpha LPS 45 kDa protease 歯周囲病原性因子マクロファージモノカイン 44kDaタンパク質 COX-2 tyrosine kinase

项目摘要

Porphyromonas gingivalis, a gram-negative anaerobe implicated in the etiology and pathogenesis of human periodontal diseases, produces a variety of potent proteolytic enzymes. In order to clarify the pathogenic roles for proteases from Porphyromonas gingivalis, 45 kDa protease was isolated from Porphyromonas gingivalis culture medium by a combination of gelfiltrations (Bio-Gel A) and ion-exchange chromatographies (DEAE-Spephacel). The enzyme was found to have a molecular mass 45 kDa by SDS-PAGE and to require mercaptoethanol for its activation. The 45 kDa protease cleaved T-kininogen into small fragments, but failed to release Kinin. The protein (2.5mug/ml) showed no stimulation activity on the productions of PGE<@D22@>D2, IL-1beta, and TNF-alphafrom the macrophages, whereas LPS (2.5mug/ml) makedly induced the productions of them from the macrophages (134.4(]SY.+-。[)51.0 PGE<@D22@>D2ng/ 10<@D16@>D1 cells ; 917 (]SY.+-。[)103IL-1beta pg/ 10<@D16@>D1 cells ; 560 (]SY.+-。[)74TNF-alpha pg/ 10<@D16@>D1 cells). These results suggest that 45KDa protease neither releases Kinin from the Kininogen nor stimulates PGE<@D22@>D2 and monokimes, implicated in the bone resorption.

牙龈卟啉单胞菌是一种革兰氏阴性厌氧菌，与人类牙周病的病因和发病机制有关，能产生多种有效的蛋白水解酶。为了阐明牙龈卟啉单胞菌的蛋白水解酶的致病作用，采用凝胶过滤(Bio-Gel A)和离子交换层析(DEAE-Spephacel)相结合的方法，从牙龈卟啉单胞菌培养基中分离出45 kDa的水解酶。经SDS-PAGE分析，该酶的相对分子质量为45 kDa，需要巯基乙醇才能激活。45 kDa的蛋白水解酶将T-激肽原切割成小片段，但不能释放激肽。该蛋白(2.5µg/ml)对巨噬细胞产生前列腺素E_(22)、白介素1(IL-1β)和肿瘤坏死因子-α(D2)无刺激作用，而内毒素(2.5µg/ml)可诱导巨噬细胞(134.4)产生上述物质。[)51.0 PGE&lt；@D22@&gt；D2 ng/10&lt；@D16@&gt；d1细胞；917()sy.+-。[)103IL-1beta PG/10&lt；@D16@&gt；D1Cells；560(]sy.+-。[)74TNF-αPG/10；d1细胞)。这些结果表明，45 KDa的蛋白水解酶既不能从激肽原释放激肽，也不能刺激与骨吸收有关的前列腺素E_(22)和D_2。