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由多粘类芽孢杆菌 JB115 产生的β-葡聚糖诱导巨噬细胞活化的机制。

Mechanism of macrophage activation induced by beta-glucan produced from Paenibacillus polymyxa JB115.

机构信息

College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2010 Jan 15;391(3):1358-62. doi: 10.1016/j.bbrc.2009.12.064. Epub 2009 Dec 21.

Abstract

Beta-glucans are heterogeneous groups of glucose polymers found in the cell walls of fungi, plants and some bacteria. Our previous report showed that a novel beta-1,3/1,6-glucan produced from Paenibacillus (P.) polymyxa JB115 can induce nitric oxide (NO) production in RAW264.7 cells. In the present study, the beta-glucan significantly increased luciferase activity in cells transfected with NFkappaB or AP1, but not STAT1, reporter vector DNA, which contain their binding promoter site. All specific NFkappaB and MAPKs pathway inhibitors (pyrrolidine dithiocarbamate, AG490, U0126, SB203580 and SP600125) remarkably attenuated NO production induced by the beta-glucan. Furthermore, Western blot analysis revealed that the stimulation of Raw264.7 cells by beta-glucan induced phosphorylation of IkappaB and the consequent translocation of NFkappaB into the nucleus. Meanwhile, phosphorylation of ERK1/2, JNK/SAPK and p38 MAPKs in cytoplasm were also confirmed. All these results indicated that beta-glucan from P. polymyxa JB115 activates macrophages through MAPKs and NFkappaB signaling pathway.

摘要

β-葡聚糖是存在于真菌、植物和某些细菌细胞壁中的葡萄糖聚合物的异质群体。我们之前的报告表明,从多粘类芽孢杆菌(P.)polymyxa JB115 中产生的一种新型β-1,3/1,6-葡聚糖可以诱导 RAW264.7 细胞产生一氧化氮(NO)。在本研究中,β-葡聚糖显著增加了转染 NFkappaB 或 AP1 报告载体 DNA 的细胞中的荧光素酶活性,但不增加包含其结合启动子位点的 STAT1 报告载体 DNA。所有特定的 NFkappaB 和 MAPKs 通路抑制剂(吡咯烷二硫代氨基甲酸盐、AG490、U0126、SB203580 和 SP600125)显著减弱了β-葡聚糖诱导的 NO 产生。此外,Western blot 分析表明,β-葡聚糖刺激 Raw264.7 细胞导致 IkappaB 磷酸化,随后 NFkappaB 易位到细胞核。同时,还证实了细胞质中 ERK1/2、JNK/SAPK 和 p38 MAPKs 的磷酸化。所有这些结果表明,来自多粘类芽孢杆菌 JB115 的β-葡聚糖通过 MAPKs 和 NFkappaB 信号通路激活巨噬细胞。

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