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

牙龈卟啉单胞菌是牙周病的主要致病菌之一。脂多糖（lipopolysaccharide，LPS）表达与骨吸收、诱导各种炎性细胞因子以及诱导牙周组织改变和破坏（包括附着丧失、胶原降解和牙槽骨损失）的牙周疾病直接相关的典型活性。LPS也具有比来自肠杆菌的LPS更温和的内毒素活性，并且能够在LPS无应答的C3 H/HeJ小鼠中激活脾细胞有丝分裂原性、从腹腔巨噬细胞释放细胞因子，其程度与LPS应答小鼠相同。然而，关于这些事实的构效关系的研究还没有完成，特别是关于Pg LPS激活LPS非应答性小鼠细胞的事实，人们非常感兴趣埃森 ...更多信息 脂A是脂多糖的活性中心，脂A本身具有生物活性，脂多糖或天然脂A制剂可诱导LPS无应答的C_3 H/HeJ小鼠腹腔巨噬细胞产生与LPS应答小鼠相同程度的细胞因子。在C3 H/HeJ小鼠的脾细胞中的促有丝分裂性和从腹腔巨噬细胞释放TNF-α和IL-6，然而天然脂质。A强烈展示了这些活动。当在LPS响应性C3 H/HeN小鼠中测量时，牙龈卟啉单胞菌的合成脂质A也显示出比用作阳性对照的大肠杆菌合成脂质A（506）所观察到的生物活性略低的生物活性。结论：牙龈卟啉单胞菌的LPS本身不能激活LPS无应答小鼠的细胞，尽管天然脂质A能够激活LPS无应答小鼠的细胞。几个研究小组报道的LPS非应答小鼠细胞对LPS或牙龈卟啉单胞菌天然脂质A的反应可能认为这些制剂中的活性物质是污染物;外膜蛋白等。少

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