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Reducing Staphylococcus aureus biofilm formation on stainless steel 316L using functionalized self-assembled monolayers
Authors:Kristen M Kruszewski  Laura Nistico  Mark J Longwell  Matthew J Hynes  Joshua A Maurer  Luanne Hall-Stoodley  Ellen S Gawalt
Affiliation:1. Duquesne University, Department of Chemistry and Biochemistry, 600 Forbes Avenue, Pittsburgh, PA 15282, USA;2. Allegheny General Hospital, Center for Genomic Sciences, Allegheny-Singer Research Institute, 320 East North Avenue, 11th floor, South Tower, Pittsburgh, PA 15212, USA;3. Washington University in St. Louis, Department of Chemistry, One Brookings Drive, St. Louis, MO 63130, USA;4. Southampton Wellcome Trust Clinical Research Facility/NIHR Respiratory BRU, University of Southampton Faculty of Medicine, Southampton General Hospital, Tremona Road, Southampton, Hampshire SO16 6YD, UK;5. Duquesne University, Department of Chemistry and Biochemistry, McGowan Institute for Regenerative Medicine, 600 Forbes Avenue, Pittsburgh, PA 15282, USA
Abstract:Stainless steel 316L (SS316L) is a common material used in orthopedic implants. Bacterial colonization of the surface and subsequent biofilm development can lead to refractory infection of the implant. Since the greatest risk of infection occurs perioperatively, strategies that reduce bacterial adhesion during this time are important. As a strategy to limit bacterial adhesion and biofilm formation on SS316L, self-assembled monolayers (SAMs) were used to modify the SS316L surface. SAMs with long alkyl chains terminated with hydrophobic (? CH3) or hydrophilic (oligoethylene glycol) tail groups were used to form coatings and in an orthogonal approach, SAMs were used to immobilize gentamicin or vancomycin on SS316L for the first time to form an “active” antimicrobial coating to inhibit early biofilm development. Modified SS316L surfaces were characterized using surface infrared spectroscopy, contact angles, MALDI-TOF mass spectrometry and atomic force microscopy. The ability of SAM-modified SS316L to retard biofilm development by Staphylococcus aureus was functionally tested using confocal scanning laser microscopy with COMSTAT image analysis, scanning electron microscopy and colony forming unit analysis. Neither hydrophobic nor hydrophilic SAMs reduced biofilm development. However, gentamicin-linked and vancomycin-linked SAMs significantly reduced S. aureus biofilm formation for up to 24 and 48 h, respectively.
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