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Title: Restructuring of Enterococcus faecalis biofilm architecture in response to antibiotic-induced stress

Bacterial biofilms are intrinsically resistant to antimicrobial treatment, which contributes to microbial persistence in clinical infections. Enterococcus faecalis is an opportunistic pathogen that readily forms biofilms and is the most prevalent enterococcal species identified in healthcare-associated infections. Since intrinsic resistance to multiple antibiotics is common for enterococci, and antibiotic resistance is elevated in biofilm populations, it is imperative to understand the mechanisms involved. Previously, we identified two glycosyltransferase genes whose disruption resulted in impaired nascent biofilm formation in the presence of antibiotic concentrations subinhibitory for parent growth and biofilm formation. The glycosyltransferases are involved in synthesis of the cell-wall-associated rhamnopolysaccharide Epa. Here we examined the effect of epa mutations on the temporal development of E. faecalis biofilms, and on the effects of antibiotics on pre-formed biofilms using scanning electron microscopy. We show that ΔepaOX mutant cells arrange into complex multidimensional biofilms independent of antibiotic exposure, while parent cells form biofilms that are monolayers in the absence of antibiotics. Remarkably, upon exposure to antibiotics parent biofilm cells restructure into complex three-dimensional biofilms resembling those of the ΔepaOX mutant without antibiotics. All biofilms exhibiting complex cellular architectures were less structurally stable than monolayer biofilms, with the biofilm cells exhibiting increased detachment. Ourmore » results indicate that E. faecalis biofilms restructure in response to cellular stress whether induced by antibiotics in the case of parent cells, or by deficiencies in Epa composition for the ΔepaOX strain. The data demonstrate a link between cellular architecture and antibiotic resistance of E. faecalis biofilms.« less
Authors:
 [1] ;  [1] ; ORCiD logo [2] ;  [1]
  1. Univ. of Minnesota, Minneapolis, MN (United States). Dept. of Microbiology and Immunology
  2. Univ. of Minnesota, Minneapolis, MN (United States). Dept. of Microbiology and Immunology. Dept. of Lab Medicine and Pathology
Publication Date:
Grant/Contract Number:
FG02-93ER20097; AI58134; AI122742; T90 DE0227232; DMR-1229263
Type:
Accepted Manuscript
Journal Name:
npj Biofilms and Microbiomes
Additional Journal Information:
Journal Volume: 3; Journal ID: ISSN 2055-5008
Publisher:
Springer Nature
Research Org:
Univ. of Minnesota, Minneapolis, MN (United States)
Sponsoring Org:
USDOE Office of Science (SC), Basic Energy Sciences (BES) (SC-22); National Inst. of Health (NIH) (United States); National Science Foundation (NSF)
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; antimicrobials; biofilms
OSTI Identifier:
1425576

Dale, Jennifer L., Nilson, Jennifer L., Barnes, Aaron M. T., and Dunny, Gary M.. Restructuring of Enterococcus faecalis biofilm architecture in response to antibiotic-induced stress. United States: N. p., Web. doi:10.1038/s41522-017-0023-4.
Dale, Jennifer L., Nilson, Jennifer L., Barnes, Aaron M. T., & Dunny, Gary M.. Restructuring of Enterococcus faecalis biofilm architecture in response to antibiotic-induced stress. United States. doi:10.1038/s41522-017-0023-4.
Dale, Jennifer L., Nilson, Jennifer L., Barnes, Aaron M. T., and Dunny, Gary M.. 2017. "Restructuring of Enterococcus faecalis biofilm architecture in response to antibiotic-induced stress". United States. doi:10.1038/s41522-017-0023-4. https://www.osti.gov/servlets/purl/1425576.
@article{osti_1425576,
title = {Restructuring of Enterococcus faecalis biofilm architecture in response to antibiotic-induced stress},
author = {Dale, Jennifer L. and Nilson, Jennifer L. and Barnes, Aaron M. T. and Dunny, Gary M.},
abstractNote = {Bacterial biofilms are intrinsically resistant to antimicrobial treatment, which contributes to microbial persistence in clinical infections. Enterococcus faecalis is an opportunistic pathogen that readily forms biofilms and is the most prevalent enterococcal species identified in healthcare-associated infections. Since intrinsic resistance to multiple antibiotics is common for enterococci, and antibiotic resistance is elevated in biofilm populations, it is imperative to understand the mechanisms involved. Previously, we identified two glycosyltransferase genes whose disruption resulted in impaired nascent biofilm formation in the presence of antibiotic concentrations subinhibitory for parent growth and biofilm formation. The glycosyltransferases are involved in synthesis of the cell-wall-associated rhamnopolysaccharide Epa. Here we examined the effect of epa mutations on the temporal development of E. faecalis biofilms, and on the effects of antibiotics on pre-formed biofilms using scanning electron microscopy. We show that ΔepaOX mutant cells arrange into complex multidimensional biofilms independent of antibiotic exposure, while parent cells form biofilms that are monolayers in the absence of antibiotics. Remarkably, upon exposure to antibiotics parent biofilm cells restructure into complex three-dimensional biofilms resembling those of the ΔepaOX mutant without antibiotics. All biofilms exhibiting complex cellular architectures were less structurally stable than monolayer biofilms, with the biofilm cells exhibiting increased detachment. Our results indicate that E. faecalis biofilms restructure in response to cellular stress whether induced by antibiotics in the case of parent cells, or by deficiencies in Epa composition for the ΔepaOX strain. The data demonstrate a link between cellular architecture and antibiotic resistance of E. faecalis biofilms.},
doi = {10.1038/s41522-017-0023-4},
journal = {npj Biofilms and Microbiomes},
number = ,
volume = 3,
place = {United States},
year = {2017},
month = {6}
}