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Both effects may help explain the higher prevalence of the comC1 allele in the pneumococcal population. Conflict of interest statement: Competing Interests: Dr. José Melo-Cristino has received research grants administered through his university and received honoraria for serving on the speakers bureaus of Pfizer, Bial, GlaxoSmithKline and Novartis. Dr. Mário Ramirez has received honoraria for serving on the speakers bureau of Pfizer and for consulting from GlaxoSmithKline. The other authors declare no conflict of interest.

No company or financing body had any interference in the decision to publish. The authors would like to declare that their stated conflicts of interest do not alter their adherence to all the PLOS ONE policies on sharing data and materials. In vitro Streptococcus mutans adhesion and biofilm formation on different OBJECTIVES: To evaluate the ability of different esthetic archwires to retain MATERIALS AND METHODS: Seven different brands of coated orthodontic archwires were tested: two epoxy coated, two polytetrafluoroethylene coated, two rhodium coated, and one silver plus polymer coated. Purchase were used as controls. Colanic acid compound mutans adherence to archwires was quantified by colony count following 24 hours of biolfilm growth, and total wire-associated biofilm was measured using a crystal violet staining assay. For both tests, two conditions were used: 0% sucrose and 3% sucrose. For statistical analysis, P < 5 was considered as statistically significant.

RESULTS: For S. mutans colony forming units per biofilm, there were no statistically significant differences among the various archwires (P = 95 for 0% sucrose; P = 05 for 3% sucrose). Regarding total biofilm formed on archwires in the 3% sucrose condition, there were statistically significant differences in crystal violet staining only for the comparison between Niti Micro Dental White and Copper Ni-Ti wires (P < 5). CONCLUSIONS: The clinical use of esthetic-coated orthodontic wires may be considered to have similar risks as uncoated archwires for biofilm retention. Involvement of Chromosomally Encoded Homologs of the RRNPP Protein Family in Enterococcus faecalis Biofilm Formation and Urinary Tract Infection Enterococcus faecalis is an opportunistic pathogen capable of causing infections, including endocarditis and urinary tract infections (UTI). One of the well-characterized quorum-sensing pathways in E. faecalis involves coordination of the conjugal transfer of pheromone-responsive plasmids by PrgX, a member of the RRNPP protein family.

Members of this protein family in various Firmicutes have also been shown to contribute to numerous cellular processes, surveyed the genome of the multidrug-resistant strain V583 for additional RRNPP homologs using computational searches and refined those identified hits for predicted structural similarities to known RRNPP family members. This led us to investigate the contribution of the chromosomally encoded RRNPP homologs to biofilm processes and pathogenesis in a catheter-associated urinary tract infection (CAUTI) model. In this study, we identified five such homologs and formation as well as outcomes in the CAUTI model.IMPORTANCEEnterococcus faecalis causes health care-associated infections and displays resistance to a variety of broad-spectrum antibiotics by acquisition of resistance traits as well as the ability to form biofilms. Even though a growing number of factors related to biofilm formation have been identified, mechanisms that contribute to biofilm formation are still largely unknown. Members of the RRNPP protein family regulate a diverse set of biological reactions in low-G+C Gram-positive bacteria Yersinia pestis biofilm in the flea vector and its role in the transmission of Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y.

pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-beta-1,6-N-acetyl-d-glucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food- and water-borne enteric pathogen from which Y.