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The study of structural factor of lipid A to mediate the activation of C3H/HeJ mice

脂质A结构因子介导C3H/HeJ小鼠活化的研究

基本信息

批准号：
09670301
负责人：
KUMADA Hidefumi
金额：
$ 1.92万
依托单位：
Kanagawa Dental College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670301/
关键词：
Porphyromonas gingivalis endotoxin synthetic lipid A Limulus amoebocyte maitogenic activity TNFalpha activity IL-6 activity C3H HeJ mouse マイトジェンリムルス IL-6 TNFα HeJマウス

项目摘要

Porphyromonas gingivalis has been implicated as one of the major periodontal pathogens. The lipopolysaccharide (LPS) expresses typical activities directly associated with the periodontal diseases of bone resorption, induction of various inflammatory cytokines, and induction of periodontal tissue alterations and destruction including attachment loss, collagen degradation and alveolar bone loss. The LPS also has a far more moderate endotoxic activity than the LPS from enterobacteria, and is able to activate splenocyte mitogenicity, cytokine release from peritoneal macrophages in LPS-nonresponsive C3H/HeJ mouse to the same extent as in LPS-responsive mouse. However, the study of the structural-activity relationship concerning these facts f is not yet done, especially, the interest is had very much about the fact in which Pg LPS activates the LPS-nonresponsive mouse cells.The lipid A part of Porphyromonas gingivalis lipopolysaccharide (LPS) was chemically synthesized to elucidate the essen … More tial activity of lipid A itself, the active center of LPS.Since the LPS or native lipid A preparation of P.gingivalis has been found to induce splenocyte mitogenicity, cytokine release from peritoneal macrophages in LPS-nonresponsive C3H/HeJ mouse to the same extent as in LPS-responsive mouse.In this study, no the synthetic lipid A of P.gingivalis certainly exhibited biological activity in the assay tested ; mitogenicity in spleen cells and the release of TNF-alpha and IL-6 from peritoneal macrophages of C3H/HeJ mouse, however the native lipid. A strongly exhibited those activities. The synthetic lipid A of P.gingivalis also exhibited biological activity a little less than those observed for Escherichia coli synthetic lipid A (506) used as a positive control, when measured those in LPS-responsive C3H/HeN mice. It was concluded that the LPS itself of P.gingivalis could not be to activate the cells of LPS-nonresponsive mouse, despite the native lipid A was able to activate. The responsibility of LPS-nonresponsive mouse cells to LPS or native lipid A of P.gingivalis reported by several groups may thought that the active material in these preparations is contaminants ; outer membrane proteins et al.. Less

牙龈卟啉单胞菌被认为是主要的牙周病原体之一。脂多糖（LPS）表达与牙周病直接相关的典型活性，包括骨吸收、诱导各种炎症细胞因子、诱导牙周组织改变和破坏，包括附着物丢失、胶原降解和牙槽骨丢失。LPS的内毒活性也比肠杆菌的内毒活性要温和得多，并且在LPS不应答的C3H/HeJ小鼠中，LPS能够激活脾细胞有丝分裂性，并在LPS应答小鼠中激活巨噬细胞释放细胞因子，其程度与LPS应答小鼠相同。然而，关于这些事实的结构-活性关系的研究尚未完成，特别是对Pg LPS激活LPS无反应的小鼠细胞的事实非常感兴趣。化学合成了牙龈卟啉单胞菌脂多糖（LPS）的脂质A部分，以阐明LPS活性中心脂质A本身的活性。由于LPS或天然脂质A制剂已被发现可诱导脾细胞有丝分裂性，因此在LPS无应答的C3H/HeJ小鼠腹膜巨噬细胞中细胞因子的释放程度与LPS应答小鼠相同。在本研究中，牙龈假单胞菌的合成脂质A在实验中没有表现出一定的生物活性；C3H/HeJ小鼠脾脏细胞的有丝分裂性和腹腔巨噬细胞tnf - α和IL-6的释放，然而天然脂质。A强烈地展示了这些活动。在lps应答的C3H/HeN小鼠中，牙龈卟啉菌合成脂质A的生物活性也略低于作为阳性对照的大肠杆菌合成脂质A（506）。结果表明，尽管天然脂质A能够激活LPS无应答小鼠的细胞，但牙龈假单胞多糖本身不能激活LPS无应答小鼠的细胞。一些研究小组报道的LPS-无应答小鼠细胞对LPS或天然脂质A的责任可能认为这些制剂中的活性物质是污染物；外膜蛋白等。少