乙型肝炎病毒表面抗原抑制TLR2 和TLR4的激活

刘华; 陈志翱; 成玉明; 袁正宏

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微生物与感染 ›› 2008, Vol. 3 ›› Issue (2) : 84-89.

论著

乙型肝炎病毒表面抗原抑制TLR2 和TLR4的激活

刘华; 陈志翱; 成玉明; 袁正宏

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HBsAg interferes with the TLR2 and TLR4 signaling pathway

LIU Hua , CHEN Zhiao , CHENG Yu-ming, YUAN Zheng-hong

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摘要

目的　研究乙型肝炎病毒表面抗原(HBsAg) 在乙型肝炎病毒逃逸机体天然免疫中的作用。方法　 PMA诱导THP-1分化成巨噬样细胞，并与乙肝表面抗原（HBsAg）共培养作比较，在LPS （TLR4配体）和pam3csk4（TLR1，2配体）的刺激下，检测细胞上清液中细胞因子IL-10，IL-12的表达及胞内IL-10，IL-12 mRNA 的含量，并利用免疫荧光观察NF-κB p65入核和Western blotting检测IκB-α蛋白降解与ERK蛋白磷酸化水平来判定TLR信号通路活化程度。结果　HBsAg的胞外处理能以剂量依赖的方式干扰pam3csk4和LPS诱导的IL-10和IL-12的产生，同时HBsAg的存在明显干扰pam3csk4和LPS诱导的NF-κB p65入核和IκB-α降解及ERK蛋白磷酸化水平。结论　HBsAg抑制TLR2和TLR4的激活。

Abstract

Objective　To investigate the role of Hepatitis B surface antigen (HBsAg) in the immune escape of innate immunity by Hepatitis B virus (HBV).　Methods After treated with PMA, THP-1 was differentiated into macrophage- like cells. Macrophage- like cells were treated further with LPS and the pam3csk4 in the presence or absence of HBsAg. Cytokine IL-10 , IL-12 protein, IL-10, IL-12 mRNA levels , NF-κB p65 protein nuclear translocation as well as IκB-α degradation and ERK protein phosphorylation were detected to monitor the activation of the TLR signaling pathway. Results LPS and the pam3csk4 induced production of cytokine IL-10 , IL-12 protein, NF-κB p65 protein nuclear translocation as well as IκB-α degradation and ERK protein phosphorylation were inhibited by HBsAg in a dose-dependent manner. Conclusion HBsAg inhibit the activation of TLR2 and TLR4 signaling pathway.

导出引用

刘华; 陈志翱; 成玉明; 袁正宏. 乙型肝炎病毒表面抗原抑制TLR2 和TLR4的激活[J]. 微生物与感染. 2008, 3(2): 84-89

LIU Hua , CHEN Zhiao , CHENG Yu-ming, YUAN Zheng-hong. HBsAg interferes with the TLR2 and TLR4 signaling pathway[J]. Journal of Microbes and Infections. 2008, 3(2): 84-89