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脂多糖刺激人单核细胞释放前列腺素E2。对从疑似牙周病原体制备的脂多糖的比较。

Lipopolysaccharide-stimulated PGE2 release from human monocytes. Comparison of lipopolysaccharides prepared from suspected periodontal pathogens.

作者信息

Garrison S W, Holt S C, Nichols F C

机构信息

Department of Periodontology, University of Connecticut, School of Dental Medicine, Farmington 06032.

出版信息

J Periodontol. 1988 Oct;59(10):684-7. doi: 10.1902/jop.1988.59.10.684.

Abstract

Lipopolysaccharides (LPS) prepared from the suspected periodontal pathogens Actinobacillus actinomycetemcomitans (A. a.), Bacteroides gingivalis, B. intermedius and Wolinella recta were compared to Salmonella typhimurium LPS for their capacity to stimulate prostaglandin E2 (PGE2) release from human monocytes. Counterflow isolated monocytes were cultured with control medium or media containing 10 micrograms/ml LPS. Media were then exchanged every 24 hours for a total of 72 hours. Salmonella and Wolinella LPS preparations demonstrated seven-fold greater PGE2 release than B. gingivalis and two-fold greater than A. a. and B. intermedius. PGE2 release was found to decrease over time with all LPS preparations except Wolinella. The potency of the LPS preparations is tentatively ranked as follows: Wolinella greater than or equal to Salmonella greater than A. a. greater than B. intermedius greater than or equal to B. gingivalis. These findings demonstrate that LPS preparations from suspected periodontal pathogens are capable of stimulating PGE2 release from human monocytes. The high potency and prolonged stimulation of PGE2 release with Wolinella LPS suggests unusual toxic properties that may exert a greater influence in the pathogenesis of destructive periodontal diseases.

摘要

将从疑似牙周病原体伴放线放线杆菌(A. a.)、牙龈拟杆菌、中间拟杆菌和直肠沃廉菌制备的脂多糖(LPS)与鼠伤寒沙门氏菌LPS相比较,以评估它们刺激人单核细胞释放前列腺素E2(PGE2)的能力。通过逆流法分离出的单核细胞与对照培养基或含有10微克/毫升LPS的培养基一起培养。然后每24小时更换一次培养基,共持续72小时。沙门氏菌和沃廉菌的LPS制剂所引起的PGE2释放量比牙龈拟杆菌高7倍,比A. a.和中间拟杆菌高2倍。除沃廉菌外,所有LPS制剂引起的PGE2释放量均随时间下降。LPS制剂的效力初步排序如下:沃廉菌≥沙门氏菌>A. a.>中间拟杆菌≥牙龈拟杆菌。这些发现表明,来自疑似牙周病原体的LPS制剂能够刺激人单核细胞释放PGE2。沃廉菌LPS对PGE2释放的高效力和长期刺激表明其具有不同寻常的毒性特性,可能在破坏性牙周疾病的发病机制中发挥更大作用。

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