Effect of L-HSL on biofilm and motility of Pseudomonas aeruginosa and its mechanism

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2024年7月16日

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Deping Tang,
Yanyan Lin,
Huihui Yao,
Yali Liu,
Yanpeng Xi,
Mengjiao Li,
Aihong Mao

摘要

Abstract

Pseudomonas aeruginosa (P. aeruginosa) biofilm formation is a crucial cause of enhanced antibiotic resistance. Quorum sensing (QS) is involved in regulating biofilm formation; QS inhibitors block the QS signaling pathway as a new strategy to address bacterial resistance. This study investigated the potential and mechanism of L-HSL (N-(3-cyclic butyrolactone)-4-trifluorophenylacetamide) as a QS inhibitor for P. aeruginosa. The results showed that L-HSL effectively inhibited the biofilm formation and dispersed the pre-formed biofilm of P. aeruginosa. The production of extracellular polysaccharides and the motility ability of P. aeruginosa were suppressed by L-HSL. C. elegans infection experiment showed that L-HSL was non-toxic and provided protection to C. elegans against P. aeruginosa infection. Transcriptomic analysis revealed that L-HSL downregulated genes related to QS pathways and biofilm formation. L-HSL exhibits a promising potential as a therapeutic drug for P. aeruginosa infection.

Key points

• Chemical synthesis of N-(3-cyclic butyrolactone)-4-trifluorophenylacetamide, named L-HSL.

• L-HSL does not generate survival pressure on the growth of P. aeruginosa and can inhibit the QS system.

• KEGG enrichment analysis found that after L-HSL treatment, QS-related genes were downregulated.