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Role of the Pre-neck Appendage Protein (Dpo7) from Phage vB_SepiS-phiIPLA7 as an Anti-biofilm Agent in Staphylococcal Species.

Authors
  • Gutiérrez, Diana1
  • Briers, Yves2
  • Rodríguez-Rubio, Lorena3
  • Martínez, Beatriz1
  • Rodríguez, Ana1
  • Lavigne, Rob4
  • García, Pilar1
  • 1 Consejo Superior de Investigaciones Científicas - Instituto de Productos Lácteos de Asturias Villaviciosa, Spain. , (Spain)
  • 2 Laboratory of Gene Technology, KU Leuven Heverlee, Belgium ; Laboratory of Applied Biotechnology, Ghent University Ghent, Belgium. , (Belgium)
  • 3 Consejo Superior de Investigaciones Científicas - Instituto de Productos Lácteos de Asturias Villaviciosa, Spain ; Laboratory of Gene Technology, KU Leuven Heverlee, Belgium. , (Belgium)
  • 4 Laboratory of Gene Technology, KU Leuven Heverlee, Belgium. , (Belgium)
Type
Published Article
Journal
Frontiers in Microbiology
Publisher
Frontiers Media SA
Publication Date
Jan 01, 2015
Volume
6
Pages
1315–1315
Identifiers
DOI: 10.3389/fmicb.2015.01315
PMID: 26635776
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Staphylococcus epidermidis and Staphylococcus aureus are important causative agents of hospital-acquired infections and bacteremia, likely due to their ability to form biofilms. The production of a dense exopolysaccharide (EPS) matrix enclosing the cells slows the penetration of antibiotic down, resulting in therapy failure. The EPS depolymerase (Dpo7) derived from bacteriophage vB_SepiS-phiIPLA7, was overexpressed in Escherichia coli and characterized. A dose dependent but time independent response was observed after treatment of staphylococcal 24 h-biofilms with Dpo7. Maximum removal (>90%) of biofilm-attached cells was obtained with 0.15 μM of Dpo7 in all polysaccharide producer strains but Dpo7 failed to eliminate polysaccharide-independent biofilm formed by S. aureus V329. Moreover, the pre-treatment of polystyrene surfaces with Dpo7 reduced the biofilm biomass by 53-85% in the 67% of the tested strains. This study supports the use of phage-encoded EPS depolymerases to prevent and disperse staphylococcal biofilms, thereby making bacteria more susceptible to the action of antimicrobials.

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