ArticleWorld journal of microbiology & biotechnology2026
An integrated in-vitro, transcriptomic, and in-silico approach to understand the molecular mechanism of quorum-sensing inhibition by Epigallocatechin-3-gallate (EGCG) in Chromobacterium violaceum.
Article in World journal of microbiology & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Sequential eradication of bacterial persisters: integrating phytochemical pharmacology with microenvironment-responsive delivery strategies.Frontiers in microbiology · 2026Review
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5 authors.
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Abstract
Quorum Sensing (QS) inhibition has become a promising strategy to fight bacterial infection since it inhibits pathogenesis without killing the bacteria. The present study has explored the anti-QS and anti-biofilm activity of Epigallocatechin-3-gallate (EGCG), a major phyto-constituent of green tea. EGCG showed a significant reduction in biofilm formation, violacein, exopolysaccharide, protease production, and swarming motility in Chromobacterium violaceum ATCC 12472 at different sub-inhibitory concentrations (25-150 µg/ml). Its efficacy was checked along with an antibiotic drug, tetracycline, with reported anti-QS potential. EGCG didn't hamper the growth of the bacterium up to 75 µg/ml concentration, but inhibited QS-related factors. Transcriptomic profiling of differentially expressed genes (DEGs) in EGCG and tetracycline-treated bacterial cells demonstrated that EGCG led to significant downregulation of QS-related genes, particularly those within the CviI/CviR circuit (cviI, cviR, and vioABCDE). In contrast, tetracycline exhibited a broader suppression of essential metabolic genes, reflecting its general bactericidal activity. Quantitative RT-PCR analysis validated that EGCG significantly reduced the expression of QS-related genes in C. violaceum. Our proposed pathway for EGCG-mediated QS inhibition pointed towards the EGCG's interaction with the CviR protein. Molecular docking and dynamic simulation studies predicted that EGCG binds stably to the CviR, potentially obstructing its interaction with the autoinducer and subsequent DNA binding. This study promotes EGCG as an effective QS inhibitor, which could help develop anti-bacterial medications targeting quorum sensing.
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