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Interaction of caffeine with the SOS response pathway in Escherichia coli

BACKGROUND: Previous studies have highlighted the antimicrobial activity of caffeine, both individually and in combination with other compounds. A proposed mechanism for caffeine’s antimicrobial effects is inhibition of bacterial DNA repair pathways. The current study examines the influence of sub-l...

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Autores principales: Whitney, Alyssa K, Weir, Tiffany L
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539924/
https://www.ncbi.nlm.nih.gov/pubmed/26288658
http://dx.doi.org/10.1186/s13099-015-0069-x
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author Whitney, Alyssa K
Weir, Tiffany L
author_facet Whitney, Alyssa K
Weir, Tiffany L
author_sort Whitney, Alyssa K
collection PubMed
description BACKGROUND: Previous studies have highlighted the antimicrobial activity of caffeine, both individually and in combination with other compounds. A proposed mechanism for caffeine’s antimicrobial effects is inhibition of bacterial DNA repair pathways. The current study examines the influence of sub-lethal caffeine levels on the growth and morphology of SOS response pathway mutants of Escherichia coli. METHODS: Growth inhibition after treatment with caffeine and methyl methane sulfonate (MMS), a mutagenic agent, was determined for E. coli mutants lacking key genes in the SOS response pathway. The persistence of caffeine’s effects was explored by examining growth and morphology of caffeine and MMS-treated bacterial isolates in the absence of selective pressure. RESULTS: Caffeine significantly reduced growth of E. coli recA- and uvrA-mutants treated with MMS. However, there was no significant difference in growth between umuC-isolates treated with MMS alone and MMS in combination with caffeine after 48 h of incubation. When recA-isolates from each treatment group were grown in untreated medium, bacterial isolates that had been exposed to MMS or MMS with caffeine showed increased growth relative to controls and caffeine-treated isolates. Morphologically, recA-isolates that had been treated with caffeine and both caffeine and MMS together had begun to display filamentous growth. CONCLUSIONS: Caffeine treatment further reduced growth of recA- and uvrA-mutants treated with MMS, despite a non-functional SOS response pathway. However, addition of caffeine had very little effect on MMS inhibition of umuC-mutants. Thus, growth inhibition of E. coli with caffeine treatment may be driven by caffeine interaction with UmuC, but also appears to induce damage by additional mechanisms as evidenced by the additive effects of caffeine in recA- and uvrA-mutants.
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spelling pubmed-45399242015-08-19 Interaction of caffeine with the SOS response pathway in Escherichia coli Whitney, Alyssa K Weir, Tiffany L Gut Pathog Research BACKGROUND: Previous studies have highlighted the antimicrobial activity of caffeine, both individually and in combination with other compounds. A proposed mechanism for caffeine’s antimicrobial effects is inhibition of bacterial DNA repair pathways. The current study examines the influence of sub-lethal caffeine levels on the growth and morphology of SOS response pathway mutants of Escherichia coli. METHODS: Growth inhibition after treatment with caffeine and methyl methane sulfonate (MMS), a mutagenic agent, was determined for E. coli mutants lacking key genes in the SOS response pathway. The persistence of caffeine’s effects was explored by examining growth and morphology of caffeine and MMS-treated bacterial isolates in the absence of selective pressure. RESULTS: Caffeine significantly reduced growth of E. coli recA- and uvrA-mutants treated with MMS. However, there was no significant difference in growth between umuC-isolates treated with MMS alone and MMS in combination with caffeine after 48 h of incubation. When recA-isolates from each treatment group were grown in untreated medium, bacterial isolates that had been exposed to MMS or MMS with caffeine showed increased growth relative to controls and caffeine-treated isolates. Morphologically, recA-isolates that had been treated with caffeine and both caffeine and MMS together had begun to display filamentous growth. CONCLUSIONS: Caffeine treatment further reduced growth of recA- and uvrA-mutants treated with MMS, despite a non-functional SOS response pathway. However, addition of caffeine had very little effect on MMS inhibition of umuC-mutants. Thus, growth inhibition of E. coli with caffeine treatment may be driven by caffeine interaction with UmuC, but also appears to induce damage by additional mechanisms as evidenced by the additive effects of caffeine in recA- and uvrA-mutants. BioMed Central 2015-08-18 /pmc/articles/PMC4539924/ /pubmed/26288658 http://dx.doi.org/10.1186/s13099-015-0069-x Text en © Whitney and Weir. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Whitney, Alyssa K
Weir, Tiffany L
Interaction of caffeine with the SOS response pathway in Escherichia coli
title Interaction of caffeine with the SOS response pathway in Escherichia coli
title_full Interaction of caffeine with the SOS response pathway in Escherichia coli
title_fullStr Interaction of caffeine with the SOS response pathway in Escherichia coli
title_full_unstemmed Interaction of caffeine with the SOS response pathway in Escherichia coli
title_short Interaction of caffeine with the SOS response pathway in Escherichia coli
title_sort interaction of caffeine with the sos response pathway in escherichia coli
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539924/
https://www.ncbi.nlm.nih.gov/pubmed/26288658
http://dx.doi.org/10.1186/s13099-015-0069-x
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