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      Statins and Antimicrobial Effects: Simvastatin as a Potential Drug against Staphylococcus aureus Biofilm

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          Abstract

          Statins are important lipid-lowering agents with other pleiotropic effects. Several studies have explored a possible protective effect of statins to reduce the morbidity and mortality of many infectious diseases. Staphylococcus aureus is one of the main pathogens implicated in nosocomial infections; its ability to form biofilms makes treatment difficult. The present study observed the MIC of atorvastatin, pravastatin and simvastatin against S. aureus, Pseudomonas aeruginosa, Escherichia coli and Enterococcus faecalis. Simvastatin was the only agent with activity against clinical isolates and reference strains of methicilin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA). Thus, the effects of simvastatin on the growth, viability and biofilm formation of S. aureus were tested. In addition, a possible synergistic effect between simvastatin and vancomycin was evaluated. Simvastatin’s MIC was 15.65 µg/mL for S. aureus 29213 and 31.25 µg/mL for the other strains of S. aureus. The effect of simvastatin was bactericidal at 4xMIC and bacteriostatic at the MIC concentration. No synergistic effect was found between simvastatin and vancomycin. However, the results obtained against S. aureus biofilms showed that, in addition to inhibiting adhesion and biofilm formation at concentrations from 1/16xMIC to 4xMIC, simvastatin was also able to act against mature biofilms, reducing cell viability and extra-polysaccharide production. In conclusion, simvastatin showed pronounced antimicrobial activity against S. aureus biofilms, reducing their formation and viability.

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          Most cited references35

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          Molecular mechanisms of antimicrobial tolerance and resistance in bacterial and fungal biofilms.

          The formation of microbial biofilms is an important reason for failure of antimicrobial therapy. However, the molecular mechanisms underlying the survival of biofilm cells are still not completely understood. In this review we discuss three mechanisms that play an important role in biofilm survival: (i) biofilm-specific protection against oxidative stress; (ii) biofilm-specific expression of efflux pumps; and (iii) protection provided by matrix polysaccharides. We demonstrate that these mechanisms are found both in bacterial and fungal biofilms and are often surprisingly similar between distantly related organisms. In addition, we give an overview of the data that suggests that these mechanisms may not be independent. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Biofilm formation and dispersal and the transmission of human pathogens.

            Several pathogenic bacterial species that are found in the environment can form complex multicellular structures on surfaces known as biofilms. Pseudomonas aeruginosa, Vibrio cholerae and certain species of nontuberculous mycobacteria are examples of human pathogens that form biofilms in natural aquatic environments. We suggest that the dynamics of biofilm formation facilitates the transmission of pathogens by providing a stable protective environment and acting as a nidus for the dissemination of large numbers of microorganisms; both as detached biofilm clumps and by the fluid-driven dispersal of biofilm clusters along surfaces. We also suggest that emerging evidence indicates that biofilm formation conveys a selective advantage to certain pathogens by increasing their ability to persist under diverse environmental conditions.
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              Statin effects beyond lipid lowering--are they clinically relevant?

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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                28 May 2015
                2015
                : 10
                : 5
                : e0128098
                Affiliations
                [1 ]Pharmacology, Anesthesiology and Therapeutics, Department of Physiological Sciences, Piracicaba Dental School, State University of Campinas, Piracicaba, São Paulo, Brazil
                [2 ]Department of General Biology, Area of Physiology and Pathophysiology, State University of Ponta Grossa, Paraná, Brazil
                [3 ]Department of Dentistry, Implantology Area, University of Santo Amaro, São Paulo, São Paulo, Brazil
                Ghent University, BELGIUM
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: TSG GCF FCG KCM. Performed the experiments: TSG MCC KCM. Analyzed the data: TSG EDA HOSF FCG KCM. Contributed reagents/materials/analysis tools: TSG MCC GCF EDA HOSF FCG KCM. Wrote the paper: TSG MCC GCF EDA HOSF FCG KCM.

                ‡ These authors also contributed equally to this work.

                Article
                PONE-D-15-00948
                10.1371/journal.pone.0128098
                4447369
                26020797
                165faa46-c124-4783-9686-36d6631001ea
                Copyright @ 2015

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                : 8 January 2015
                : 23 April 2015
                Page count
                Figures: 5, Tables: 3, Pages: 17
                Funding
                Financial support was provided by http://www.fapesp.br/en/, FAPESP -São Paulo Research Foundation Grant - 2013/06570-3 (KCM) and Master fellowship - 2011/15795-3 (TSG); http://www.cnpq.br/, The Brazilian National Council for Scientific and Technological Development - CNPq Graduation fellowship- PIBIC (MCC).
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