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伴放线放线杆菌的脂多糖与小鼠巨噬细胞J774中一氧化氮的产生

LPS from Actinobacillus actinomycetemcomitans and production of nitric oxide in murine macrophages J774.

作者信息

Blix I J, Helgeland K

机构信息

Department of Oral Biology, Faculty of Dentistry, University of Oslo, Blindern, Norway.

出版信息

Eur J Oral Sci. 1998 Feb;106(1):576-81. doi: 10.1046/j.0909-8836.1998.eos106107.x.

DOI:10.1046/j.0909-8836.1998.eos106107.x
PMID:9527358
Abstract

Nitric oxide (NO) plays a complex role in the modulation of the inflammatory response, having either a pro-inflammatory or a protective role. Actinobacillus actinomycetemcomitans is considered an important etiological agent in localized juvenile periodontitis. We have studied the effect of lipopolysaccharide (LPS) extracted from this periodontopathogenic bacterium on NO synthesis in an in vitro murine macrophage system. LPS from A. actinomycetemcomitans induced a significant production of NO even at concentrations as low as 1 ng/ml, whereas LPS from E. coli had to be added in concentrations of 100 ng/ml to obtain similar effects. Production of NO was blocked by NG-nitro-L-arginine methylester, and pre-treatment of LPS from A. actinomycetemcomitans with polymyxin B abolished the production of NO, while prostaglandin E2 enhanced the synthesis of NO.

摘要

一氧化氮(NO)在炎症反应调节中发挥着复杂作用,具有促炎或保护作用。伴放线放线杆菌被认为是局限性青少年牙周炎的重要病原体。我们研究了从这种牙周致病菌中提取的脂多糖(LPS)对体外小鼠巨噬细胞系统中NO合成的影响。伴放线放线杆菌的LPS即使在低至1 ng/ml的浓度下也能诱导显著的NO产生,而大肠杆菌的LPS必须以100 ng/ml的浓度添加才能获得类似效果。NO的产生被NG-硝基-L-精氨酸甲酯阻断,用多粘菌素B预处理伴放线放线杆菌的LPS可消除NO的产生,而前列腺素E2可增强NO的合成。

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