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LsrR 在乳腺致病性大肠杆菌生物膜形成中的调控作用。

Role of LsrR in the regulation of biofilm formation in mammary pathogenic Escherichia coli.

机构信息

School of Life Sciences, Anhui Agricultural University, Hefei,, Anhui, 230036, China.

出版信息

BMC Vet Res. 2024 May 23;20(1):220. doi: 10.1186/s12917-024-04086-9.

Abstract

BACKGROUND

Mammary Pathogenic Escherichia coli (MPEC) is an important pathogen that can escape the attack of the host immune system through biofilm formation and proliferate in the mammary gland continuously, resulting in mastitis in cows and causing enormous economic losses. As an effector of AI-2 quorum sensing, LsrR extensively affects the expression levels of hundreds of genes related to multiple biological processes in model E. coli strain. However, the regulatory role of LsrR in MPEC and whether it is involved in pathogenesis has been seldom reported.

RESULTS

In this study, the function of LsrR in strain MPEC5, obtained from a milk sample in dairy cows with mastitis, was investigated by performing high-throughput sequencing (RNA-seq) assays. The results revealed that LsrR down-regulated the transcript levels of fimAICDFGH (encoding Type 1 pili), which have been reported to be associated with biofilm formation process. Biofilm assays confirmed that deletion of lsrR resulted in a significant increase in biofilm formation in vitro. In addition, electrophoretic mobility shift assay (EMSA) provided evidence that LsrR protein could directly bind to the promoter regions of fimAICDFGH in a dose-dependent manner.

CONCLUSIONS

These results indicate that LsrR protein inhibits the biofilm formation ability of MPEC5 by directly binding to the fimAICDFGH promoter region. This study presents a novel clue for further exploration of the prevention and treatment of MPEC.

摘要

背景

乳腺致病性大肠杆菌(MPEC)是一种重要的病原体,它可以通过形成生物膜来逃避宿主免疫系统的攻击,并在乳腺中持续增殖,导致奶牛乳腺炎,并造成巨大的经济损失。作为 AI-2 群体感应的效应物,LsrR 广泛影响模型大肠杆菌菌株中与多种生物过程相关的数百个基因的表达水平。然而,LsrR 在 MPEC 中的调控作用及其是否参与发病机制尚未得到充分报道。

结果

在本研究中,通过高通量测序(RNA-seq)实验,研究了来自乳腺炎奶牛奶样的 MPEC5 菌株中 LsrR 的功能。结果表明,LsrR 下调了 fimAICDFGH(编码 I 型菌毛)的转录水平,而 fimAICDFGH 已被报道与生物膜形成过程有关。生物膜实验证实,lsrR 缺失导致体外生物膜形成显著增加。此外,电泳迁移率变动分析(EMSA)提供了证据表明,LsrR 蛋白可以以剂量依赖的方式直接结合 fimAICDFGH 的启动子区域。

结论

这些结果表明,LsrR 蛋白通过直接结合 fimAICDFGH 启动子区域抑制 MPEC5 的生物膜形成能力。本研究为进一步探索 MPEC 的防治提供了新的线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ef/11112850/460b1b66bda1/12917_2024_4086_Fig1_HTML.jpg

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