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伴放线放线杆菌荚膜物质对成纤维细胞增殖和胶原蛋白合成的抑制作用

Inhibition of fibroblast proliferation and collagen synthesis by capsular material from Actinobacillus actinomycetemcomitans.

作者信息

Kamin S, Harvey W, Wilson M, Scutt A

出版信息

J Med Microbiol. 1986 Nov;22(3):245-9. doi: 10.1099/00222615-22-3-245.

Abstract

Cytotoxic effects of bacteria found in dental plaque are usually attributed to lipopolysaccharides (LPS) or ill-defined toxins. Many bacteria implicated in periodontal disease produce surface exopolymers (capsules) recently shown to stimulate bone resorption. Capsular material and LPS extracted from Actinobacillus (Haemophilus) actinomycetemcomitans were purified and examined for their effects on cultures of human gingival fibroblasts. DNA and collagen synthesis were significantly inhibited by capsular material (0.1-50 micrograms/ml). LPS caused only modest inhibition of DNA synthesis at 10 and 50 micrograms/ml, and had no effect on collagen synthesis. Release of lactate dehydrogenase from fibroblasts was not increased by LPS nor by capsular material, showing that the inhibitory effects were not due to cell death. Capsular material, but not LPS, caused a pronounced increase in cell size; a doubling of the nuclear area occurred within 72 h exposure. These results indicate that the capsule of A. actinomycetemcomitans may play an active role in the tissue destruction characterising inflammatory periodontal disease.

摘要

牙菌斑中发现的细菌的细胞毒性作用通常归因于脂多糖(LPS)或不明毒素。许多与牙周病有关的细菌会产生表面胞外聚合物(荚膜),最近发现这些聚合物会刺激骨吸收。从伴放线放线杆菌(放线杆菌属)中提取的荚膜物质和LPS被纯化,并检测它们对人牙龈成纤维细胞培养物的影响。荚膜物质(0.1 - 50微克/毫升)显著抑制DNA和胶原蛋白合成。LPS在10和50微克/毫升时仅对DNA合成有适度抑制,对胶原蛋白合成无影响。LPS和荚膜物质均未增加成纤维细胞中乳酸脱氢酶的释放,表明抑制作用并非由于细胞死亡。荚膜物质而非LPS导致细胞大小显著增加;在暴露72小时内细胞核面积加倍。这些结果表明,伴放线放线杆菌的荚膜可能在表征炎症性牙周病的组织破坏中起积极作用。

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