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Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression
Resveratrol exhibits a potent antimicrobial activity. However, the mechanism underlying its antibacterial activity has not been shown. In this study, the antibacterial mechanism of resveratrol was investigated. To investigate induction of the SOS response, a strain containing the lacZ(+)gene under t...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419592/ https://www.ncbi.nlm.nih.gov/pubmed/25942564 http://dx.doi.org/10.1038/srep10029 |
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author | Hwang, Dahyun Lim, Young-Hee |
author_facet | Hwang, Dahyun Lim, Young-Hee |
author_sort | Hwang, Dahyun |
collection | PubMed |
description | Resveratrol exhibits a potent antimicrobial activity. However, the mechanism underlying its antibacterial activity has not been shown. In this study, the antibacterial mechanism of resveratrol was investigated. To investigate induction of the SOS response, a strain containing the lacZ(+)gene under the control of an SOS-inducible sulA promoter was constructed. DNA damage was measured by pulse-field gel electrophoresis (PFGE). After resveratrol treatment, the cells were observed by confocal microscopy. For the RNA silencing assay, ftsZ-specific antisense peptide nucleic acid (PNA) was used. Reactive oxygen species (ROS) production increased in Escherichia coli after resveratrol treatment; however, cell growth was not recovered by ROS quenching, indicating that, in this experiment, ROS formation and cell death following resveratrol treatment were not directly correlated. Resveratrol treatment increased DNA fragmentation in cells, while SOS response-related gene expression levels increased in a dose-dependent manner. Cell elongation was observed after resveratrol treatment. Elongation was induced by inhibiting FtsZ, an essential cell-division protein in prokaryotes, and resulted in significant inhibition of Z-ring the formation in E. coli. The expression of ftsZ mRNA was suppressed by resveratrol. Our results indicate that resveratrol inhibits bacterial cell growth by suppressing FtsZ expression and Z-ring formation. |
format | Online Article Text |
id | pubmed-4419592 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-44195922015-05-18 Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression Hwang, Dahyun Lim, Young-Hee Sci Rep Article Resveratrol exhibits a potent antimicrobial activity. However, the mechanism underlying its antibacterial activity has not been shown. In this study, the antibacterial mechanism of resveratrol was investigated. To investigate induction of the SOS response, a strain containing the lacZ(+)gene under the control of an SOS-inducible sulA promoter was constructed. DNA damage was measured by pulse-field gel electrophoresis (PFGE). After resveratrol treatment, the cells were observed by confocal microscopy. For the RNA silencing assay, ftsZ-specific antisense peptide nucleic acid (PNA) was used. Reactive oxygen species (ROS) production increased in Escherichia coli after resveratrol treatment; however, cell growth was not recovered by ROS quenching, indicating that, in this experiment, ROS formation and cell death following resveratrol treatment were not directly correlated. Resveratrol treatment increased DNA fragmentation in cells, while SOS response-related gene expression levels increased in a dose-dependent manner. Cell elongation was observed after resveratrol treatment. Elongation was induced by inhibiting FtsZ, an essential cell-division protein in prokaryotes, and resulted in significant inhibition of Z-ring the formation in E. coli. The expression of ftsZ mRNA was suppressed by resveratrol. Our results indicate that resveratrol inhibits bacterial cell growth by suppressing FtsZ expression and Z-ring formation. Nature Publishing Group 2015-05-05 /pmc/articles/PMC4419592/ /pubmed/25942564 http://dx.doi.org/10.1038/srep10029 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Hwang, Dahyun Lim, Young-Hee Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title | Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title_full | Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title_fullStr | Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title_full_unstemmed | Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title_short | Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression |
title_sort | resveratrol antibacterial activity against escherichia coli is mediated by z-ring formation inhibition via suppression of ftsz expression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419592/ https://www.ncbi.nlm.nih.gov/pubmed/25942564 http://dx.doi.org/10.1038/srep10029 |
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