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感染诱导小鼠巨噬细胞释放高迁移率族蛋白B1。

Infection Induces High Mobility Group Box 1 Released from Mouse Macrophages.

作者信息

Wang Hui, Li Muzi, Liu Jing, Xu Jianhai, Han Qian, Liu Qun

机构信息

National Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, China.

Department of Pathogenic Biology, Chengdu Medical CollegeChengdu, China.

出版信息

Front Microbiol. 2017 Apr 24;8:658. doi: 10.3389/fmicb.2017.00658. eCollection 2017.

Abstract

High mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular. causes inflammatory pathological changes including ileitis and encephalitis in chronic infection. To investigate whether HMGB1 contributes to the toxoplasmosis lesions, we examined HMGB1 changes during infection. The results showed that HMGB1 transcription was down-regulated in the murine macrophage ANA1 cell line and mouse peritoneal macrophages (PMΦs) after inoculation, but up-regulated in the IFN-γ treated macrophages and the intraperitoneal exudate cells from the infected mice. The content of intracellular HMGB1 are basically consistent with the transcription levels in ANA1 assay, while there were no obvious changes in the mouse PMΦs. Both ANA1 and mouse PMΦs released HMGB1 after parasites infection, and no obvious HMGB1 aggregation in cytoplasm compare to the IFN-γ treatment group. Furthermore, we demonstrated that invasion led to HMGB1 release, which was dependent on the Caspase 1 activity. These finding should promote to further investigate the functions of extracellular HMGB1 in the toxoplasmosis.

摘要

高迁移率族蛋白B1(HMGB1)在细胞内大量表达并具有DNA结合能力。然而,更重要的是,当它释放到细胞外时,它是一种通过促炎反应和免疫调节来对抗感染的武器。在慢性感染中会导致包括回肠炎和脑炎在内的炎症性病理变化。为了研究HMGB1是否促成弓形虫病病变,我们检测了感染期间HMGB1的变化。结果显示,接种后,小鼠巨噬细胞ANA1细胞系和小鼠腹腔巨噬细胞(PMΦs)中HMGB1转录下调,但在经γ干扰素处理的巨噬细胞和来自感染小鼠的腹腔渗出细胞中上调。在ANA1检测中,细胞内HMGB1的含量与转录水平基本一致,而在小鼠PMΦs中没有明显变化。寄生虫感染后,ANA1和小鼠PMΦs均释放HMGB1,与γ干扰素处理组相比,细胞质中没有明显的HMGB1聚集。此外,我们证明弓形虫入侵导致HMGB1释放,这依赖于半胱天冬酶1的活性。这些发现应有助于进一步研究细胞外HMGB1在弓形虫病中的功能。

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