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Conflict of interest statement: Competing Interests: GSC has recieved finanical support to attend meetings from Novacta Biosystems. CHC has recieved financial support to attend meetings from Astellas. JF has received financial support to attend meetings from Bayer and Wyeth. [https://en.wikipedia.org/wiki/Colanic_acid Order immediately] has received financial support to attend meetings from Bayer and Targenta Therapeutics. MHW has received honoraria consultancy work, financial support to attend meetings and research funding from does not alter the authors' adherence to PLOS ONE policies on sharing data and Abolition of biofilm formation in urinary tract Escherichia coli and Klebsiella isolates by metal interference through competition for fur. Bacterial biofilms are associated with a large number of persistent and chronic infections.<br /><br /> Biofilm-dwelling bacteria are particularly resistant to antibiotics and immune defenses, which makes it hard if not impossible to eradicate biofilm-associated infections. In the urinary tract, free iron is strictly limited but is critical for bacterial growth. Biofilm-associated Escherichia coli cells are particularly desperate for iron. An attractive way of inhibiting biofilm formation is to fool the bacterial regulatory system for iron uptake. Here, we demonstrate that biofilm formation can be impaired by the addition of divalent metal ions, such as Zn(II) and Co(II), which inhibit iron uptake by virtue of their higher-than-iron affinity for the master controller protein of strains in the presence of Zn(II) was observed in microtiter plates and flow chambers as well as on urinary catheters. These results further support that iron uptake is indeed crucial for biofilm formation, and thereby, targeting these uptake systems might be an effective way to eradicate biofilms caused by Sustained prevention of biofilm formation on a novel silicone matrix suitable Bacterial colonization and biofilm formation on medical devices constitute major challenges in clinical long-term use of e.g.<br /><br /> [http://www.allinno.com/product/food/684.html Colanic acid compound] to the risk of risking bacterial resistance development. The aim of the present project was to introduce a novel antibacterial approach involving an advanced composite material applicable for medical devices. The polymeric composites investigated consisted of a hydrogel network of cross-linked poly(2-hydroxyethyl methacrylate) (PHEMA) embedded in a poly(dimethylsiloxane) (PDMS) silicone elastomer produced using supercritical carbon dioxide (scCO2). In these materials, the hydrogel may contain an active pharmaceutical ingredient while the silicone elastomer provides the sufficient mechanical stability of the material. In these conceptual studies, the antimicrobial agent ciprofloxacin was loaded into the polymer matrix by a post-polymerization loading procedure. Sustained release of ciprofloxacin was demonstrated, and the release could be controlled by varying the hydrogel content in the range 13-38% (w/w) and by changing the concentration of ciprofloxacin during loading in the range of 1-20mg/mL. Devices containing 25% (w/w) hydrogel and loaded with ciprofloxacin displayed a strong antibacterial effect against Staphylococcus aureus bacterial colonization and subsequent biofilm formation on the device material was inhibited for 29days.<br /><br /> In conclusion, the hydrogel/silicone composite represents a promising candidate material for medical devices that prevent bacterial Design of an anti-adhesive surface by a pilicide strategy. Biofilm formation on surfaces is one of major problems in medical, cosmetic and research of new strategies to inhibit biofilm formation is urgent. Recently, virstatin, which interferes with bacterial type IV pili formation, has demonstrated a capacity to inhibit biofilm formation developed by Acinetobacter baumannii after 24h. In this study, we aim to elaborate anti-adhesive surfaces preventing biofilm development by the covalent immobilization of virstatin on silicon surface. Surfaces were functionalized by self-assembled monolayers of two aminosilanes (11-aminoundecyltrimethoxysilane (AUTMS) and 3-aminopropyltrimethoxysilane (APTMS)). Then, virstatin (2mM) was immobilized on those modified surfaces. We observed an increase in surface hydrophobicity of AUTMS modified substratum leading to an increase of A.<br /><br /> baumannii ATCC 17978 adhesion (after 4h). Immobilization of virstatin molecule on APTMS modified surface was efficient to decrease cell attachment by 32±5% compared to unmodified surface. As virstatin is known to inhibit type IV pili formation in solution, the observed decrease of bacterial adhesion might be due to this pilicide action.