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转录组分析揭示小蛋白 MgtS 有助于尿路致病性大肠杆菌的毒力。

Transcriptomic analysis reveals that the small protein MgtS contributes to the virulence of uropathogenic Escherichia coli.

机构信息

Tianjin Key Laboratory of Microbial Functional Genomics, TEDA College, Nankai University, Tianjin, 300457, China; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China.

Tianjin Key Laboratory of Microbial Functional Genomics, TEDA College, Nankai University, Tianjin, 300457, China; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China.

出版信息

Microb Pathog. 2021 Mar;152:104765. doi: 10.1016/j.micpath.2021.104765. Epub 2021 Jan 29.

DOI:10.1016/j.micpath.2021.104765
PMID:33524567
Abstract

Uropathogenic Escherichia coli (UPEC) is the most common pathogen causing urinary tract infections (UTIs). The pathogenesis of UPEC relies on the formation of intracellular bacterial communities (IBCs) after invading bladder epithelial cells (BECs). In this study, the gene expression profiles of UPEC after invading BECs were comprehensively analyzed using RNA sequencing to reveal potential virulence-related genes. The small protein MgtS, which is transcriptionally upregulated in BECs, was further investigated. It was found that MgtS contributed positively to UPEC invasion of BECs and colonization in murine bladders. A two-component regulatory system, PhoPQ was confirmed as a direct activator of mgtS expression in BECs, and magnesium limitation is proposed as a host cue for the activation. This study provides the first comprehensive analysis of the transcriptome profile of UPEC during its intra-BECs life, revealing a new virulence-associated gene and its regulatory mechanism.

摘要

尿路致病性大肠杆菌(UPEC)是引起尿路感染(UTIs)的最常见病原体。UPEC 的发病机制依赖于其在入侵膀胱上皮细胞(BECs)后形成细胞内细菌群落(IBCs)。在这项研究中,使用 RNA 测序全面分析了 UPEC 入侵 BEC 后的基因表达谱,以揭示潜在的与毒力相关的基因。在 BECs 中转录上调的小蛋白 MgtS 进一步进行了研究。结果发现,MgtS 有助于 UPEC 入侵 BECs 并在小鼠膀胱中定植。证实双组分调节系统 PhoPQ 是 BECs 中 mgtS 表达的直接激活物,并提出镁限制是激活的宿主信号。本研究首次对 UPEC 在其细胞内生命过程中的转录组谱进行了全面分析,揭示了一个新的与毒力相关的基因及其调控机制。

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