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由拟杆菌属、梭杆菌属和韦荣球菌属的脂多糖,以及梭杆菌属脂多糖的脂质A和多糖部分刺激引起的骨吸收。

Bone resorption stimulated by lipopolysaccharides from Bacteroides, Fusobacterium and Veillonella, and by the lipid A and the polysaccharide part of Fusobacterium lipopolysaccharide.

作者信息

Sveen K, Skaug N

出版信息

Scand J Dent Res. 1980 Dec;88(6):535-42. doi: 10.1111/j.1600-0722.1980.tb01264.x.

Abstract

Lipopolysaccharides (LPS) isolated from oral strains of Veillonella, Fusobacterium and Bacteroides stimulated the release of 45Ca from prelabeled fetal rat bones in culture. There was a typical dose-response relationship between the quantities of released 45Ca and LPS used for stimulation. Bacteroides-LPS proved to be the less active inducer of 45Ca release. LPS had no stimulating effect on the release of 45Ca from devitalized bone. The stimulated 45Ca release was paralleled by an increase in the culture medium of hydroxyproline and lactate. This, together with the findings of numerous osteoclasts in stained histological specimens of the experimental bones, indicates that LPS stimulated the osteoclasts to bone resorption. Heparin, which did not directly induce 45Ca release, potentiated the bone resorption stimulating capability of LPS. The lipid A and the polysaccharide portion of Fusobacterium LPS also stimulated bone resorption and, remarkably, the polysaccharide portion showed the greatest activity. This may explain the mode of action of LPS lacking a typical lipid A. It is suggested that stimulation of osteoclasts by LPS may result from activation of complement components by lipid A or its polysaccharide portion.

摘要

从韦荣球菌属、梭杆菌属和拟杆菌属的口腔菌株中分离出的脂多糖(LPS),刺激了培养的预先标记的胎鼠骨骼中45Ca的释放。释放的45Ca量与用于刺激的LPS量之间存在典型的剂量反应关系。事实证明,拟杆菌属LPS是45Ca释放活性较低的诱导剂。LPS对失活骨骼中45Ca的释放没有刺激作用。45Ca的释放增加的同时,培养基中的羟脯氨酸和乳酸含量也增加。这一点,再加上实验骨骼的染色组织学标本中有大量破骨细胞的发现,表明LPS刺激破骨细胞进行骨吸收。肝素本身并不直接诱导45Ca释放,但能增强LPS刺激骨吸收的能力。梭杆菌属LPS的脂质A和多糖部分也能刺激骨吸收,值得注意的是,多糖部分表现出最大的活性。这可能解释了缺乏典型脂质A的LPS的作用方式。有人认为,LPS对破骨细胞的刺激可能是由脂质A或其多糖部分激活补体成分所致。

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