Staphylococcus Epidermidis Research Paper - pinsoftek.com Custom Academic Help

Staphylococcus Epidermidis Research Paper

Staphylococcus Epidermidis Research Paper - fantasy

How to Cite this Article Abstract Plants have been an important source of secondary metabolites known for their diverse biological activities; some have been shown to inhibit the development of certain pathogenic microorganisms. Herein, the antimicrobial activity of the carbon tetrachloride, hexane, ethanol, and aqueous extracts of leaves of Stevia rebaudiana Bertoni against Staphylococcus aureus strain , Staphylococcus epidermidis strains , , and , and Pseudomonas aeruginosa strains RO3 and RO4 was presented. The antibacterial activity was evaluated using the disk diffusion method, and the minimal inhibitory concentration MIC was determined. The results show that, even at the lowest evaluated concentration 1. The aqueous extract exhibited high inhibition values These results indicate that compounds contained in non-polar extracts of S. Key words: Stevia rebaudiana, antimicrobial properties, plant extracts. Staphylococcus Epidermidis Research Paper Staphylococcus Epidermidis Research Paper

Search Menu Abstract Antibiotic-resistant pathogens often escape antimicrobial treatment by forming protective biofilms in response to quorum-sensing communication via diffusible autoinducers. Here, we present a high-throughput screening platform for small-molecular inhibitors of either enzyme.

Staphylococcus Epidermidis Research Paper

This platform employs a cell-based assay to report non-toxic, bioavailable and cell-penetrating inhibitors of AI-2 production, utilizing engineered human cells programmed to constitutively secrete AI-2 by tapping into the endogenous methylation cycle via ectopic expression of codon-optimized MTAN and LuxS.

Screening of a library of over commercial compounds yielded 66 hits, including the FDA-licensed cytostatic anti-cancer drug 5-fluorouracil 5-FU.

INTRODUCTION

Secondary screening and validation studies showed that 5-FU is a potent quorum-quencher, inhibiting AI-2 production and release by MRSA, Staphylococcus epidermidis, Escherichia coli and Vibrio harveyi. Furthermore, 5-FU reestablished antibiotic susceptibility and enabled daptomycin-mediated prevention and clearance of MRSA infection in a mouse model of human implant-associated infection.

Staphylococcus Epidermidis Research Paper

The most common quorum-sensing communication signal is autoinducer-2 AI-2 23which controls virulence and biofilm formation in various human pathogens, such as methicillin-resistant Staphylococcus aureus MRSAthereby contributing to their antibiotic resistance 4. This Paaper calls for immediate 8 and concerted action to develop alternative treatment options that can replace or complement antibiotics 9.

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Screening for enzyme-inhibiting compounds is standard practice in continue reading discovery and development, and typically involves microscale activity assays 16Staphylococcus Epidermidis Research Paper shuffling in nanocompartments 17 and virtual screening methods However, most of these in-vitro strategies provide little Staphylococcus Epidermidis Research Paper no information on the function, toxicity, bioactivity and bioavailability of the hit compounds and most hits will fail during later stages of drug development On the other hand, human cell-based assays may provide an all-in-one opportunity to detect bioavailable, cell-permeable, non-cytotoxic and target-specific functional drug candidates 20— Prime examples would be the anti-tuberculosis drugs that are currently being validated by a Bioversys-GlaxoSmithKline consortium in phase-I clinical trials Administration of 5-FU triggers apoptosis of rapidly dividing cancer cells by depriving them of dTMP.

Notably, we found that one of the hit compounds, 5-FU, blocks quorum-sensing by MRSA and prevents biofilm formation at an order-of-magnitude-lower concentration than that clinically relevant for anti-cancer therapy. Furthermore, 5-FU enables daptomycin-mediated prevention and clearance of MRSA infection in a mouse model of human implant-associated infections.]

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