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SdiA在非典型致病性大肠杆菌生物膜形成中的作用

Role of SdiA on Biofilm Formation by Atypical Enteropathogenic Escherichia coli.

作者信息

Culler Hebert F, Couto Samuel C F, Higa Juliana S, Ruiz Renato M, Yang Min J, Bueris Vanessa, Franzolin Marcia R, Sircili Marcelo P

机构信息

Laboratory of Genetics, Butantan Institute, São Paulo 05503-900, Brazil.

Laboratory of Bacteriology, Butantan Institute, São Paulo 05503-900, Brazil.

出版信息

Genes (Basel). 2018 May 15;9(5):253. doi: 10.3390/genes9050253.

Abstract

Atypical enteropathogenic are capable to form biofilm on biotic and abiotic surfaces, regardless of the adherence pattern displayed. Several mechanisms are regulated by Quorum sensing (QS), including virulence factors and biofilm formation. Quorum sensing is a signaling system that confers bacteria with the ability to respond to chemical molecules known as autoinducers. Suppressor of division inhibitor (SdiA) is a QS receptor present in atypical enteropathogenic (aEPEC) that detects acyl homoserine lactone (AHL) type autoinducers. However, these bacteria do not encode an AHL synthase, but they are capable of sensing AHL molecules produced by other species, establishing an inter-species bacterial communication. In this study, we performed experiments to evaluate pellicle, ring-like structure and biofilm formation on wild type, mutants and complemented strains. We also evaluated the transcription of genes involved in different stages of biofilm formation, such as , , , and The mutants were capable of forming thicker biofilm structures and showed increased motility when compared to wild type and complemented strains. Moreover, they also showed denser pellicles and ring-like structures. Quantitative real-time PCR (qRT-PCR) analysis demonstrated increased and transcription on mutant strains. Biofilm formation, as well as , and transcription decreased on wild type strains by the addition of AHL. These results indicate that SdiA participates on the regulation of these phenotypes in aEPEC and that AHL addition enhances the repressor effect of this receptor on the transcription of biofilm and motility related genes.

摘要

非典型肠道致病性大肠杆菌能够在生物和非生物表面形成生物膜,无论其表现出何种粘附模式。几种机制受群体感应(QS)调控,包括毒力因子和生物膜形成。群体感应是一种信号系统,赋予细菌对称为自诱导物的化学分子作出反应的能力。分裂抑制因子抑制剂(SdiA)是存在于非典型肠道致病性大肠杆菌(aEPEC)中的一种群体感应受体,可检测酰基高丝氨酸内酯(AHL)型自诱导物。然而,这些细菌不编码AHL合酶,但它们能够感知其他物种产生的AHL分子,从而建立种间细菌通讯。在本研究中,我们进行了实验,以评估野生型、突变体和互补菌株上的菌膜、环状结构和生物膜形成。我们还评估了参与生物膜形成不同阶段的基因的转录,如、、、和。与野生型和互补菌株相比,突变体能够形成更厚的生物膜结构,并表现出更高的运动性。此外,它们还表现出更致密的菌膜和环状结构。定量实时PCR(qRT-PCR)分析表明,突变菌株上和的转录增加。通过添加AHL,野生型菌株上的生物膜形成以及、和的转录减少。这些结果表明,SdiA参与aEPEC中这些表型的调控,并且添加AHL增强了该受体对生物膜和运动相关基因转录的抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e221/5977193/3467f8e7c025/genes-09-00253-g001.jpg

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