Food-Safe Modification of Stainless Steel Food-Processing Surfaces to Reduce Bacterial Biofilms
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Biofilm formation on stainless steel (SS) surfaces of food-processing plants, leading to food-borne illness outbreaks, is enabled by the attachment and confinement of pathogens within microscale cavities of surface roughness (grooves, scratches). We report foodsafe oil-based slippery coatings (FOSCs) for food-processing surfaces that suppress bacterial adherence and biofilm formation by trapping residual oil lubricant within these surface cavities to block microbial growth. SS surfaces were chemically functionalized with alkylphosphonic acid to preferentially wet a layer of food-grade oil. FOSCs reduced the effective surface roughness, the adhesion of organic food residue, and bacteria. FOSCs significantly reduced Pseudomonas aeruginosa biofilm formation on standard roughness SS-316 by 5 log CFU cm–2, and by 3 log CFU cm–2 for mirror-finished SS. FOSCs also enhanced surface cleanability, which we measured by bacterial counts after conventional detergent cleaning. Importantly, both SS grades maintained their antibiofilm activity after the erosion of the oil layer by surface wear with glass beads, which suggests that there is a residual volume of oil that remains to block surface cavity defects. These results indicate the potential of such low-cost, scalable approaches to enhance the cleanability of SS food-processing surfaces and improve food safety by reducing biofilm growth.Keywords:
Residual oil
Streptococcus sanguinis
Surface Modification
This chapter focuses on the contribution of the genome sequence of Streptococcus sanguinis to enhance one's understanding of its interactions in the oral cavity. It was determined that streptococci resembling S. sanguinis constituted about half of the streptococcal component of dental plaque. This study likely identified as S. sanguinis some strains that would currently be classified as Streptococcus oralis or Streptococcus gordonii. This chapter points out that studies with related species may provide a framework for future hypothesis-driven investigation of S. sanguinis cell wall-anchored (Cwa) proteins associated with oral adhesion and aggregation. It was later determined that competence is upregulated in S. sanguinis in the presence of oxygen, as is also true for S. pneumoniae and S. mutans. The chapter concludes with the hope that the availability of the genome sequence stimulates new research related to the role of S. sanguinis within the oral community.
Streptococcus sanguinis
Streptococcus gordonii
Streptococcus oralis
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Abstract Background Bacteria survive in various environments by forming biofilms. Bacterial biofilms often cause significant problems to medical instruments and industrial processes. Techniques to inhibit biofilm formation are essential and have wide applications. In this study, we evaluated the ability of two types of biosurfactants (rhamnolipids and surfactin) to inhibit growth and biofilm formation ability of oral pathogenic bacteria such as Aggregatibacter actinomycetemcomitans , Streptococcus mutans , and Streptococcus sanguinis . Results Rhamnolipids inhibited the growth and biofilm formation ability of all examined oral bacteria. Surfactin showed effective inhibition against S. sanguinis ATCC10556, but lower effects toward A. actinomycetemcomitans Y4 and S. mutans UA159. To corroborate these results, biofilms were observed by scanning electron microscopy (SEM) and confocal microscopy. The observations were largely in concordance with the biofilm assay results. We also attempted to determine the step in the biofilm formation process that was inhibited by biosurfactants. The results clearly demonstrated that rhamnolipids inhibit biofilm formation after the initiation process, however, they do not affect attachment or maturation. Conclusions Rhamnolipids inhibit oral bacterial growth and biofilm formation by A. actinomycetemcomitans Y4, and may serve as novel oral drug against localized invasive periodontitis.
Aggregatibacter actinomycetemcomitans
Streptococcus sanguinis
Oral Microbiome
Dental plaque
Surfactin
Bacterial growth
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This paper presented the influence of Al(III) on biodegradability, micromorphology, composition and functional groups characteristics of the biofilm extracellular polymeric substances (EPS) during different growth phases. The sequencing batch biofilm reactors were developed to cultivate biofilms under different Al(III) dosages. The results elucidated that Al(III) affected biofilm development adversely at the beginning of biofilm growth, but promoted the biofilm mass and improved the biofilm activity with the growth of the biofilm. The micromorphological observation indicated that Al(III) led to a reduction of the filaments and promotion of the EPS secretion in growth phases of the biofilm, also Al(III) could promote microorganisms to form larger colonies for mature biofilm. Then, the analysis of EPS contents and components suggested that Al(III) could increase the protein (PN) of tightly bound EPS (TB-EPS) which alleviated the metal toxicity inhibition on the biofilm during the initial phases of biofilm growth. The biofilm could gradually adapt to the inhibition caused by Al(III) at the biofilm maturation moment. Finally, through the Fourier transform infrared spectroscopy, it was found that Al(III) was beneficial for the proliferation and secretion of TB-EPS functional groups, especially the functional groups of protein and polysaccharides.
Extracellular polymeric substance
Bacterial growth
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Abstract Porphyromonas gingivalis is a keystone pathogen in periodontitis, and Streptococcus sanguinis is an abundant oral commensal bacterium associated with periodontal health. However, the interaction between P. gingivalis and S. sanguinis remains obscure. Here, we established a strategy for high‐throughput measurement of the cell number of P. gingivalis in the coculture with S. sanguinis by detecting the concentration of hydrogen sulfate. The interaction between P. gingivalis and over 2000 S. sanguinis single‐gene mutants was characterized using this strategy, and several interaction‐associated genes in S. sanguinis were determined by detecting more P. gingivalis cells in the coculture with matched S. sanguinis mutants. Three S. sanguinis interaction‐associated genes were predicted to be responsible for cysteine metabolism, and the supplementation of exogenous L‐cysteine promoted the cell number of P. gingivalis in the coculture with S. sanguinis . Thus, exogenous L‐cysteine and the compromised cysteine metabolism in S. sanguinis enhanced the growth of P. gingivalis in the existence of S. sanguinis . Additionally, the interaction between P. gingivalis and other Streptococcus spp. was examined, and S. pneumoniae was the only streptococci that had no inhibition on the cell number of P. gingivalis . In total, this study established a new strategy for high‐throughput screening of the interaction between Streptococcus and P. gingivalis and discovered a set of genes in S. sanguinis that impacted the interaction. The influence of exogenous L‐cysteine on the interaction between P. gingivalis and S. sanguinis in the oral cavity needs further investigation.
Streptococcus sanguinis
Streptococcus gordonii
Calais
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Oral Diseases (2012) 18, 586–594 Objective: To assess the effect of two oral bacteria Streptococcus sanguinis and Porphyromonas gingivalis upon platelet aggregation. Materials and Methods: Streptococcus sanguinis , P. gingivalis , S. sanguniis + P. gingivalis were added to platelet‐rich plasma and platelet aggregation measured using a platelet aggregometer. Platelets were passed through a flow chamber with S. sanguinis , P. gingivalis or a biofilm of S. sanguinis and P. gingivalis coated with saliva. Platelet adhesion to the chamber was observed under a fluorescence microscope for 15 min. The positive control was platelets treated with adrenaline; the negative control was platelets treated with phosphate‐buffered saline. Results: The mean (± s.e.) aggregation magnitude of S. sanguinis and P. gingivalis was 77.7 ± 7.4% and 79.3 ± 9.9%, respectively. The aggregation magnitude of S. sanguinis + P. gingivalis was 51.3 ± 12.9%, which was significantly lower than that for S. sanguinis / P. gingivalis ( P < 0.05). In the flow chamber system, platelets adhered to S. sanguinis/P.gingivalis respectively within 3 min, and reached a plateau at 5–15 min. Under the condition of the S. sanguinis‐ and P. gingivalis ‐saliva biofilm, platelet adhesion to the biofilm was significantly reduced at 5–15 min ( P < 0.05). Conclusions: In the static or dynamic flow system, platelets adhered to S. sanguinis or P. gingivalis . However, if S. sanguinis was mixed with P. gingivalis , the aggregation magnitude (%) was significantly reduced.
Streptococcus sanguinis
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Background Combating dental biofilm formation is the most effective means for the prevention of caries, one of the most widespread human diseases. Among the chemical supplements to mechanical tooth cleaning procedures, non-bactericidal adjuncts that target the mechanisms of bacterial biofilm formation have gained increasing interest in recent years. Milk proteins, such as lactoferrin, have been shown to interfere with bacterial colonization of saliva-coated surfaces. We here study the effect of bovine milk osteopontin (OPN), a highly phosphorylated whey glycoprotein, on a multispecies in vitro model of dental biofilm. While considerable research effort focuses on the interaction of OPN with mammalian cells, there are no data investigating the influence of OPN on bacterial biofilms. Methodology/Principal Findings Biofilms consisting of Streptococcus oralis, Actinomyces naeslundii, Streptococcus mitis, Streptococcus downei and Streptococcus sanguinis were grown in a flow cell system that permitted in situ microscopic analysis. Crystal violet staining showed significantly less biofilm formation in the presence of OPN, as compared to biofilms grown without OPN or biofilms grown in the presence of caseinoglycomacropeptide, another phosphorylated milk protein. Confocal microscopy revealed that OPN bound to the surface of bacterial cells and reduced mechanical stability of the biofilms without affecting cell viability. The bacterial composition of the biofilms, determined by fluorescence in situ hybridization, changed considerably in the presence of OPN. In particular, colonization of S. mitis, the best biofilm former in the model, was reduced dramatically. Conclusions/Significance OPN strongly reduces the amount of biofilm formed in a well-defined laboratory model of acidogenic dental biofilm. If a similar effect can be observed in vivo, OPN might serve as a valuable adjunct to mechanical tooth cleaning procedures.
Streptococcus mitis
Streptococcus oralis
Streptococcus sanguinis
Actinomyces naeslundii
Streptococcus gordonii
Osteopontin
Dental plaque
Exopolymer
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Introduction. Bacterial cell hydrophobicity and adherence to a substrate are one of the most important factors in biofilm formation. Group A streptococcus is an unstable and low biofilm productor. Importance of biofilm production in streptococcal pathogenesis is still unknown. Objective. The aim of this study was to determine the impact of hydrophobicity and adherence on the biofilm production of group A streptococcal invasive and noninvasive isolates, and also to evaluate the stability of biofilm production in time function. Methods. Adherence, hydrophobicity and biofilm production were investigated in a total of 172 isolates divided into three groups: noninvasive, low invasive and highly invasive. Adherence to uncoated and laminin-coated microtiter plates and biofilm production after 12, 24 and 48 hours of incubation was determined using the method described by Stepanovic et al. Hydrophobicity was measured using the MATH test by Rosenberg and SAT test by Lindhal. Results. Correlation between adherence and biofilm production was detected in the group of noninvasive isolates. These isolates were stable biofilm productors during all three time periods of biofilm production. In the groups of invasive and noninvasive isolates no statistical correlation was detected among the analysed variables. The invasive isolates were unstable biofilm productors. Conclusion. Noninvasive isolates were stable biofilm producers; as detected, they showed a direct correlation between adherence and biofilm production, and a negative impact of hydrophobicity on the biofilm production. Invasive isolates were unstable biofilm productors; it was observed that there was no correlation between adherence and hydrophobicity with biofilm production.
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Homoserine
Extracellular polymeric substance
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