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• W2801156774 abstract "Abstract Staphylococcus aureus is a major cause of nosocomial infections and secretes a diverse spectrum of virulence determinants as well as forms biofilm. The emergence of antibiotic-resistant S . aureus highlights the need for alternative forms of therapeutics other than conventional antibiotics. One route to meet this need is screening small molecule derivatives for potential anti-infective activity. Using a previously optimized C . elegans – S . aureus small molecule screen, we identified a benzimidazole derivative, UM-C162, which rescued nematodes from a S . aureus infection. UM-C162 prevented the formation of biofilm in a dose-dependent manner without interfering with bacterial viability. To examine the effect of UM-C162 on the expression of S . aureus virulence genes, a genome-wide transcriptome analysis was performed on UM-C162-treated pathogen. Our data indicated that the genes associated with biofilm formation, particularly those involved in bacterial attachment, were suppressed in UM-C162-treated bacteria. Additionally, a set of genes encoding vital S . aureus virulence factors were also down-regulated in the presence of UM-C162. Further biochemical analysis validated that UM-C162-mediated disruption of S . aureus hemolysins, proteases and clumping factors production. Collectively, our findings propose that UM-C162 is a promising compound that can be further developed as an anti-virulence agent to control S . aureus infections." @default.
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• W2801156774 date "2018-02-09" @default.
• W2801156774 modified "2023-10-17" @default.
• W2801156774 title "Suppression of Staphylococcus aureus biofilm formation and virulence by a benzimidazole derivative, UM-C162" @default.
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• W2801156774 doi "https://doi.org/10.1038/s41598-018-21141-2" @default.
• W2801156774 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5807447" @default.
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