ArticleBMC microbiology2025
Dihydromyricetin alleviates ETEC K88-induced intestinal inflammatory injury by inhibiting quorum sensing-related virulence factors.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Review of the Composition and Antimicrobial Roles of Extracts of Vine Tea (Ampelopsis grossedentata).Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Gut-Protective and Multifunctional Exopolysaccharide fromNutrients · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundEnterotoxigenic Escherichia coli (ETEC) is responsible for piglet diarrhea and causes substantial economic loss in the pig industry. Along with the restriction of antibiotics, natural compounds targeting bacterial virulence factors are supposed to be efficacious and attractive alternatives for controlling ETEC infection. This study aimed to investigate the influence of dihydromyricetin (DMY), a natural flavonoid compound, on the expression of virulence factors of ETEC and intestinal inflammatory injury.
resultsDMY interfered with the quorum sensing (QS) of ETEC K88 since it decreased AI-2 secretion and downregulated the expression of LuxS and Pfs, which dominate AI-2 production, and decreased the expression mRNA level of genes (lsrA, lsrB, lsrC, lsrD, lsrK, and lsrR) that are involved in AI-2 internalization and signal transduction. Additionally, DMY markedly dampened the expression of QS-related virulence genes (elt-1, estB, fliC, faeG), biofilm formation, cell adhesion, and stress tolerance of ETEC K88. Furthermore, DMY treatment applied to the ETEC K88 infection in mice model resulted in decreased amount of heat-labile (LT) and heat-stable (ST) enterotoxins, reduced production of cAMP and cGMP, downregulated protein level of CFTR and upregulated expression of NHE3 in the ileum. In addition, the mRNA expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and histological damage in the ileum were significantly decreased by DMY treatment.
conclusionsDMY can inhibit the AI-2 QS and virulence factor expression, thereby attenuating the virulence of ETEC and alleviating intestinal inflammatory damage in ETEC K88-challenged mice. This study indicated that DMY has the potential to be a promising antivirulence agent for combating ETEC infection.
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