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

牙龈卟啉单胞菌已被实施为主要的牙周病原体之一。脂多糖（LPS）表达与骨骼分辨率，各种炎性细胞因子诱导的牙周疾病以及牙周组织改变和破坏的典型活性，包括附着损失，胶原蛋白降解和肺泡骨损失。 LPS还具有比肠杆菌中LP的现代性内毒素活性要更现代的，并且能够激活脾细胞有丝分裂性，在LPS-非溶质性C3H/HEJ小鼠中从腹膜巨噬细胞中释放的细胞因子释放，其程度与LPS响应性小鼠相同。 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 essential … More tial activity of lipid A itself, the active center of LPS.Since the LPS或天然脂质的A制剂已被发现诱导脾细胞有丝分裂，在LPS-非响应性C3H/HEJ小鼠中从腹膜巨噬细胞中释放的细胞因子释放，与LPS响应性小鼠相同的程度。脾细胞中的有丝分裂性以及从C3H/HEJ小鼠的腹膜巨噬细胞中释放TNF-Alpha和IL-6，但天然脂质。强烈暴露了这些活动。吉利亚菌的合成脂质A还比大肠杆菌合成脂质A（506）所观察到的生物学活性少得多，当测量LPS反应性C3H/HEN小鼠中时。得出的结论是，LPS本身不可能激活LPS-非响应小鼠的细胞，希望天然脂质A能够激活。 LPS非反应小鼠细胞对lps或lp的脂质a的责任是多个组报告的，可能认为这些制剂中的活性物质是污染物。外膜蛋白等。