Propolis-derived components act against Klebsiella pneumoniae by inhibiting growth and disrupting biofilms.

Abstract

Aims: Klebsiella pneumoniae (K. pneumoniae), a multidrug-resistant opportunistic pathogen implicated in pneumonia and nosocomial infections, employs biofilm formation to evade antimicrobial therapies.

Methods: This study investigates how propolis and its key bioactive constituents-naringenin, taxifolin, syringic acid, and gallic acid-disrupt biofilm development and stability in K. pneumoniae. Biofilm inhibition was evaluated using crystal violet staining, adhesion assays, and scanning electron microscopy (SEM), while membrane integrity was assessed via LDH release and Live/Dead fluorescence. Molecular docking predicted interactions between compounds and biofilm-associated proteins, complemented by qRT-PCR analysis of virulence genes (fimH, ompA, mrkA, mrkD).

Results: All compounds demonstrated dose-dependent antibiofilm effects, with propolis showing superior efficacy (79.1% biofilm inhibition at 2 MIC). Propolis and its components reduced bacterial adhesion by 50%-81%, disrupted extracellular matrix architecture, and increased non-viable cell ratios (Live/Dead: 30.55% dead cells in taxifolin-treated biofilms). Taxifolin exhibited the strongest binding affinity (-7.8 kcal·mol-1) for the OmpA protein. Gene expression analysis showed that propolis, naringenin, taxifolin, and gallic acid substantially downregulated biofilm-associated genes, including fimH, ompA, mrkA, and mrkD.

Conclusions: Propolis disrupts K. pneumoniae biofilm formation via multi-target regulation, with taxifolin as a potential key bioactive monomer. The results demonstrate the potential of propolis and its main active components to inhibit K. pneumoniae.