Suppr超能文献

支原体上调 Rab7 和抑制自噬降解的协同作用促进了细胞内支原体感染。

Synergism between upregulation of Rab7 and inhibition of autophagic degradation caused by mycoplasma facilitates intracellular mycoplasma infection.

机构信息

Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.

First People's Hospital of Jiujiang City, Jiujiang, Jiangxi 330300, P.R. China.

出版信息

Mol Med Rep. 2014 Mar;9(3):793-800. doi: 10.3892/mmr.2014.1907. Epub 2014 Jan 20.

Abstract

Following fusion of a mycoplasma with a host cell membrane, the inserted components of mycoplasma may then be transported through the endocytic pathway. However, the effects of mycoplasmas on the host cell endomembrane system are largely unknown. In this study, mycoplasma‑induced changes in the dynamics of endocytic and autophagic systems were investigated. Endocytosis and autophagy are two major processes involved in the survival of intracellular prokaryotic pathogens. It was found that, immediately following infection, mycoplasmas induce endocytosis in the host cell; however, in the long term the mycoplasmas suppress turnover of the components of the endocytic pathway. Immunofluorescence microscopy revealed that Rab7 and LC3‑II are recruited to the intracellular mycoplasma‑containing compartments. Western blot analysis and quantitative reverse transcription-polymerase chain reaction (qPCR) showed that mycoplasmas increase expression of Rab7 by upregulating transcription, but increase levels of LC3‑II and p62 by post‑translational regulation. Furthermore, it was demonstrated that mycoplasma infection causes inhibition of autophagic degradation of LC3‑II and p62. In addition, it was found that upregulation of Rab7 and inhibition of autophagic degradation synergistically contributes to intracellular mycoplasma accumulation. In conclusion, these findings suggest that mycoplasmas may manipulate host cell endosomal and autophagic systems in order to facilitate intracellular infection.

摘要

在支原体与宿主细胞膜融合后,支原体插入的成分随后可能通过内吞作用途径运输。然而,支原体对宿主细胞内膜系统的影响在很大程度上尚不清楚。在本研究中,研究了支原体诱导的内吞作用和自噬系统动力学变化。内吞作用和自噬作用是涉及细胞内原核病原体存活的两个主要过程。研究发现,支原体感染后立即诱导宿主细胞的内吞作用;然而,从长远来看,支原体抑制内吞作用途径成分的周转率。免疫荧光显微镜显示 Rab7 和 LC3-II 被募集到细胞内含有支原体的隔室。Western blot 分析和定量逆转录聚合酶链反应 (qPCR) 显示,支原体通过上调转录增加 Rab7 的表达,但通过翻译后调节增加 LC3-II 和 p62 的水平。此外,研究表明支原体感染导致 LC3-II 和 p62 的自噬降解抑制。此外,研究发现 Rab7 的上调和自噬降解的抑制协同作用有助于细胞内支原体的积累。总之,这些发现表明支原体可能操纵宿主细胞内体和自噬系统,以促进细胞内感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4aef/3926517/88029f8d5eaf/MMR-09-03-0793-g00.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验