scholarly journals Controlling biofilm formation with nitroxide functional surfaces

2019 ◽  
Vol 10 (31) ◽  
pp. 4252-4258 ◽  
Author(s):  
Hendrik Woehlk ◽  
Michael J. Trimble ◽  
Sarah C. Mansour ◽  
Daniel Pletzer ◽  
Vanessa Trouillet ◽  
...  

Nitroxide functional polymer coatings with inherent antibiofilm activity are introduced as an avenue to combat bacterial biofilm contamination of medical devices.

Author(s):  
B.D. Tall ◽  
K.S. George ◽  
R. T. Gray ◽  
H.N. Williams

Studies of bacterial behavior in many environments have shown that most organisms attach to surfaces, forming communities of microcolonies called biofilms. In contaminated medical devices, biofilms may serve both as reservoirs and as inocula for the initiation of infections. Recently, there has been much concern about the potential of dental units to transmit infections. Because the mechanisms of biofilm formation are ill-defined, we investigated the behavior and formation of a biofilm associated with tubing leading to the water syringe of a dental unit over a period of 1 month.


Pathogens ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 93 ◽  
Author(s):  
Riau ◽  
Aung ◽  
Setiawan ◽  
Yang ◽  
Yam ◽  
...  

: Bacterial biofilm on medical devices is difficult to eradicate. Many have capitalized the anti-infective capability of silver ions (Ag+) by incorporating nano-silver (nAg) in a biodegradable coating, which is then laid on polymeric medical devices. However, such coating can be subjected to premature dissolution, particularly in harsh diseased tissue microenvironment, leading to rapid nAg clearance. It stands to reason that impregnating nAg directly onto the device, at the surface, is a more ideal solution. We tested this concept for a corneal prosthesis by immobilizing nAg and nano-hydroxyapatite (nHAp) on poly(methyl methacrylate), and tested its biocompatibility with human stromal cells and antimicrobial performance against biofilm-forming pathogens, Pseudomonas aeruginosa and Staphylococcus aureus. Three different dual-functionalized substrates—high Ag (referred to as 75:25 HAp:Ag); intermediate Ag (95:5 HAp:Ag); and low Ag (99:1 HAp:Ag) were studied. The 75:25 HAp:Ag was effective in inhibiting biofilm formation, but was cytotoxic. The 95:5 HAp:Ag showed the best selectivity among the three substrates; it prevented biofilm formation of both pathogens and had excellent biocompatibility. The coating was also effective in eliminating non-adherent bacteria in the culture media. However, a 28-day incubation in artificial tear fluid revealed a ~40% reduction in Ag+ release, compared to freshly-coated substrates. The reduction affected the inhibition of S. aureus growth, but not the P. aeruginosa. Our findings suggest that Ag+ released from surface-immobilized nAg diminishes over time and becomes less effective in suppressing biofilm formation of Gram-positive bacteria, such as S. aureus. This advocates the coating, more as a protection against perioperative and early postoperative infections, and less as a long-term preventive solution.


Materials ◽  
2021 ◽  
Vol 14 (7) ◽  
pp. 1704
Author(s):  
Krzysztof Pałka ◽  
Małgorzata Miazga-Karska ◽  
Joanna Pawłat ◽  
Joanna Kleczewska ◽  
Agata Przekora

The aim of this study was to evaluate the effect of modification with liquid rubber on the adhesion to tooth tissues (enamel, dentin), wettability and ability to inhibit bacterial biofilm formation of resin-based dental composites. Two commercial composites (Flow-Art–flow type with 60% ceramic filler and Boston–packable type with 78% ceramic filler; both from Arkona Laboratorium Farmakologii Stomatologicznej, Nasutów, Poland) were modified by addition of 5% by weight (of resin) of a liquid methacrylate-terminated polybutadiene. Results showed that modification of the flow type composite significantly (p < 0.05) increased the shear bond strength values by 17% for enamel and by 33% for dentine. Addition of liquid rubber significantly (p < 0.05) reduced also hydrophilicity of the dental materials since the water contact angle was increased from 81–83° to 87–89°. Interestingly, modified packable type material showed improved antibiofilm activity against Steptococcus mutans and Streptococcus sanguinis (quantitative assay with crystal violet), but also cytotoxicity against eukaryotic cells since cell viability was reduced to 37% as proven in a direct-contact WST-8 test. Introduction of the same modification to the flow type material significantly improved its antibiofilm properties (biofilm reduction by approximately 6% compared to the unmodified material, p < 0.05) without cytotoxic effects against human fibroblasts (cell viability near 100%). Thus, modified flow type composite may be considered as a candidate to be used as restorative material since it exhibits both nontoxicity and antibiofilm properties.


2019 ◽  
Vol 18 (24) ◽  
pp. 2068-2079 ◽  
Author(s):  
Michele Ciulla ◽  
Antonio Di Stefano ◽  
Lisa Marinelli ◽  
Ivana Cacciatore ◽  
Giuseppe Di Biase

S. aureus under the biofilm mode of growth is often related to several nosocomial infections, more frequently associated with indwelling medical devices (catheters, prostheses, portacaths or heart valves). As a biofilm, the biopolymer matrix provides an excellent growth medium, increasing the tolerance to antibiotics and host immune system. To date, the antimicrobial therapy alone is not effective. A novel strategy to prevent biofilm formation is based on the interference with the bacterial cell–cell communication, a process known as quorum sensing (QS) and mediated by the RNA-III-activating peptide (RAP) and its target protein TRAP (Target of RAP). The RNAIII inhibiting peptide (RIP) is able to inhibit S. aureus pathogenesis by disrupting QS mechanism competing with RAP, thus inhibiting the phosphorylation of TRAP. This alteration leads to a reduced adhesion and to the inhibition of RNAIII synthesis, with the subsequent suppression of toxins synthesis. The present paper will provide an overview on the activity and potential applications of RIP as biofilm inhibiting compound, useful in the management of S. aureus biofilm infections. Moreover, medicinal chemistry strategies have been examined to better understand which modifications and/or structure alterations were able to produce new derivatives of this QS inhibitor with an improved antibiofilm activity.


Author(s):  
Ewa Brzozowska ◽  
Anna Pyra ◽  
Krzysztof Pawlik ◽  
Sabina Górska ◽  
Andrzej Gamian

Background: Dual function tail tubular proteins (TTP) belonging to the lytic bacteriophages are the interesting group of biologically active enzymes. Surprisingly, apart from their structural function, they are also polysaccharide hydrolyzes destroying bacterial extracellular components. One of the representatives of this group is TTPB from Klebsiella pneumoniae phage &ndash; KP32. TTPB hydrolyzes exopolysaccharide (EPS) of Klebsiella pneumoniae and Enterococcus faecalis strain. This depolymerizing feature was associated with the activity to prevent bacterial biofilm formation. TTPB can inhibit biofilm formation by K. pneumoniae, Enterobacter cloacae, Staphylococcus aureus, Enterococcus faecalis and Pseudomonas aeruginosa strains. Moreover, synergistic activity with antibiotic action has been observed, most likely due to depolymerases&rsquo; facilitation of contact of antibiotic with bacterial cells. Methods: TTPB was overexpressed in E coli system, purified and tested towards the bacterial strains using agar overlay method. The hydrolytic activity of TTPB was performed using EPSs of K. pneumoniae PCM2713 and E. cloacae ATCC 13047 as the substrates. Next, we determined the reducing sugar (RS) levels in the TTPB/EPS mixtures, regarding the RS amount obtained after acidic hydrolysis. The antibiofilm activity of TTPB has been set down on bacterial biofilm using a biochemical method. Finally, we have demonstrated the synergistic activity of TTPB with kanamycin. Results: For the first time, the hydrolytic activity of TTPB towards bacterial EPSs has been shown. TTPB releases about a half of the whole RS amount of EPSs belonging to K. pneumoniae PCM 2713 and E. cloacae ATCC 13047 strains. 1.12 &micro;M of the phage protein reduces biofilm of both strains by over 60%. Destroying the bacterial biofilm the phage protein improves the antibiotic action increasing kanamycin effectiveness up to four times.


2015 ◽  
Vol 82 (1) ◽  
pp. 394-401 ◽  
Author(s):  
Jakub Kwiecinski ◽  
Manli Na ◽  
Anders Jarneborn ◽  
Gunnar Jacobsson ◽  
Marijke Peetermans ◽  
...  

ABSTRACTStaphylococcus aureusbiofilm infections of indwelling medical devices are a major medical challenge because of their high prevalence and antibiotic resistance. As fibrin plays an important role inS. aureusbiofilm formation, we hypothesize that coating of the implant surface with fibrinolytic agents can be used as a new method of antibiofilm prophylaxis. The effect of tissue plasminogen activator (tPA) coating onS. aureusbiofilm formation was tested within vitromicroplate biofilm assays and anin vivomouse model of biofilm infection. tPA coating efficiently inhibited biofilm formation by variousS. aureusstrains. The effect was dependent on plasminogen activation by tPA, leading to subsequent local fibrin cleavage. A tPA coating on implant surfaces prevented both early adhesion and later biomass accumulation. Furthermore, tPA coating increased the susceptibility of biofilm infections to antibiotics.In vivo, significantly fewer bacteria were detected on the surfaces of implants coated with tPA than on control implants from mice treated with cloxacillin. Fibrinolytic coatings (e.g., with tPA) reduceS. aureusbiofilm formation bothin vitroandin vivo, suggesting a novel way to prevent bacterial biofilm infections of indwelling medical devices.


2021 ◽  
Vol 12 ◽  
Author(s):  
Donald C. Hall ◽  
Phillip Palmer ◽  
Hai-Feng Ji ◽  
Garth D. Ehrlich ◽  
Jarosław E. Król

Recent advances in 3D printing have led to a rise in the use of 3D printed materials in prosthetics and external medical devices. These devices, while inexpensive, have not been adequately studied for their ability to resist biofouling and biofilm buildup. Bacterial biofilms are a major cause of biofouling in the medical field and, therefore, hospital-acquired, and medical device infections. These surface-attached bacteria are highly recalcitrant to conventional antimicrobial agents and result in chronic infections. During the COVID-19 pandemic, the U.S. Food and Drug Administration and medical officials have considered 3D printed medical devices as alternatives to conventional devices, due to manufacturing shortages. This abundant use of 3D printed devices in the medical fields warrants studies to assess the ability of different microorganisms to attach and colonize to such surfaces. In this study, we describe methods to determine bacterial biofouling and biofilm formation on 3D printed materials. We explored the biofilm-forming ability of multiple opportunistic pathogens commonly found on the human body including Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus to colonize eight commonly used polylactic acid (PLA) polymers. Biofilm quantification, surface topography, digital optical microscopy, and 3D projections were employed to better understand the bacterial attachment to 3D printed surfaces. We found that biofilm formation depends on surface structure, hydrophobicity, and that there was a wide range of antimicrobial properties among the tested polymers. We compared our tested materials with commercially available antimicrobial PLA polymers.


2020 ◽  
Vol 29 (Sup4) ◽  
pp. S25-S35
Author(s):  
Pornanong Aramwit ◽  
Supamas Napavichayanum ◽  
Prompong Pienpinijtham ◽  
Yousef Rasmi ◽  
Nipaporn Bang

Objective: To investigate the potential of sericin extracted by different methods to inhibit biofilm formation (prevention) and disrupt already formed biofilm (treatment). Method: In this in vitro study, sericin was extracted by heat, acid, alkali and urea. Streptococcus mutans bacteria were cultivated in the presence of various concentrations of sericin to evaluate antibiofilm formation using cell density assay (inhibition effect before biofilm formed). Conversely, various concentrations of sericin were added to a biofilm already formed by Streptococcus mutans bacteria, and the viability of bacteria assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay (disruption effects after biofilm formed). Structures of extracted sericin were evaluated using circular dichroism and Fourier-transform infrared spectrometer. Results: The urea-extracted sericin at all concentrations (12.5mg/ml, 25mg/ml, 50mg/ml and 100mg/ml) showed the highest potential antibiofilm activity in terms of both inhibition and disruption effects, compared with sericin extracted by heat, acid or alkali. The heat-extracted and acid-extracted sericin were found to reduce the biofilm formation dose-dependently, while the alkali-extracted sericin did not show either inhibition or disruption effect on the bacterial biofilm. The urea-extracted sericin also killed the bacteria residing within the biofilm, possibly due to its modified structure which may destabilise the bacterial cell wall, leading to membrane disintegration and, finally, cell death. Conclusion: Our results demostrated the antibiofilm activity of sericin. This could form the basis of further research on the mechanism and application of sericin as a novel antibiofilm agent.


2014 ◽  
Vol 58 (9) ◽  
pp. 5395-5404 ◽  
Author(s):  
Katrijn De Brucker ◽  
Nicolas Delattin ◽  
Stijn Robijns ◽  
Hans Steenackers ◽  
Natalie Verstraeten ◽  
...  

ABSTRACTWe identified a 26-amino-acid truncated form of the 34-amino-acid cathelicidin-related antimicrobial peptide (CRAMP) in the islets of Langerhans of the murine pancreas. This peptide, P318, shares 67% identity with the LL-37 human antimicrobial peptide. As LL-37 displays antimicrobial and antibiofilm activity, we tested antifungal and antibiofilm activity of P318 against the fungal pathogenCandida albicans. P318 shows biofilm-specific activity as it inhibitsC. albicansbiofilm formation at 0.15 μM without affecting planktonic survival at that concentration. Next, we tested theC. albicansbiofilm-inhibitory activity of a series of truncated and alanine-substituted derivatives of P318. Based on the biofilm-inhibitory activity of these derivatives and the length of the peptides, we decided to synthesize the shortened alanine-substituted peptide at position 10 (AS10; KLKKIAQKIKNFFQKLVP). AS10 inhibitedC. albicansbiofilm formation at 0.22 μM and acted synergistically with amphotericin B and caspofungin against mature biofilms. AS10 also inhibited biofilm formation of different bacteria as well as of fungi and bacteria in a mixed biofilm. In addition, AS10 does not affect the viability or functionality of different cell types involved in osseointegration of an implant, pointing to the potential of AS10 for further development as a lead peptide to coat implants.


2022 ◽  
Vol 12 ◽  
Author(s):  
Lulin Rao ◽  
Yaoguang Sheng ◽  
Jiao Zhang ◽  
Yanlei Xu ◽  
Jingyi Yu ◽  
...  

The resistance of methicillin-resistant Staphylococcus aureus (MRSA) has augmented due to the abuse of antibiotics, bringing about difficulties in the treatment of infection especially with the formation of biofilm. Thus, it is essential to develop antimicrobials. Here we synthesized a novel small-molecule compound, which we termed SYG-180-2-2 (C21H16N2OSe), that had antibiofilm activity. The aim of this study was to demonstrate the antibiofilm effect of SYG-180-2-2 against clinical MRSA isolates at a subinhibitory concentration (4 μg/ml). In this study, it was showed that significant suppression in biofilm formation occurred with SYG-180-2-2 treatment, the inhibition ranged between 65.0 and 85.2%. Subsequently, confocal laser scanning microscopy and a bacterial biofilm metabolism activity assay further demonstrated that SYG-180-2-2 could suppress biofilm. Additionally, SYG-180-2-2 reduced bacterial adhesion and polysaccharide intercellular adhesin (PIA) production. It was found that the expression of icaA and other biofilm-related genes were downregulated as evaluated by RT-qPCR. At the same time, icaR and codY were upregulated when biofilms were treated with SYG-180-2-2. Based on the above results, we speculate that SYG-180-2-2 inhibits the formation of biofilm by affecting cell adhesion and the expression of genes related to PIA production. Above all, SYG-180-2-2 had no toxic effects on human normal alveolar epithelial cells BEAS-2B. Collectively, the small-molecule compound SYG-180-2-2 is a safe and effective antibacterial agent for inhibiting MRSA biofilm.


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