Microbial pathogenesis · 2026
2H-chromen-2-one disrupts the Staphylococcus aureus biofilm matrix and potentiates moxifloxacin activity: In vitro and in silico analyses.
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Khanh Le Ngoc, Anh Nguyen Thi Lan, Quynh Nguyen Thi Nhu, Nguyen Thanh Tung, Ho Duc Viet, Hoai Nguyen Thi, Huong Phung Thanh, Nguyen Tiep Khac
Аннотация
OBJECTIVES: Staphylococcus aureus biofilms contribute to antimicrobial tolerance and treatment failure, motivating the search for antibiofilm adjuvants that restore antibiotic activity. In this study, we evaluated 2H-chromen-2-one isolated from Aspidistra letrea for its antibiofilm activity and its ability to potentiate moxifloxacin (MXF) against S. aureus biofilms.
METHODS: Established biofilms were quantified by total biomass (crystal violet staining) and viable bacteria (CFU enumeration) following exposure to 2H-chromen-2-one alone or in combination with MXF, including testing MXF at a clinically relevant peak concentration (Cmax). Molecular docking was performed against proteins encoded by the ica locus to explore potential molecular targets.
RESULTS: 2H-chromen-2-one reduced biofilm biomass by approximately 50% at 1-2 mg/mL and markedly increased MXF antibiofilm killing in a concentration-dependent manner. Notably, MXF alone showed minimal killing at Cmax, whereas co-treatment achieved a reduction of up to approximately 1.6 log10 CFU/mL (>97% killing) and reduced the bactericidal concentration requirement from >1.5 to 0.032 mg/L. Moreover, the maximal reduction efficacy of MXF increased from approximately -2 log10 CFU/mL when MXF was used alone to approximately -3 log10 CFU/mL when combined with 2H-chromen-2-one. Docking suggested a putative interaction between 2H-chromen-2-one and IcaC, consistent with interference in poly-N-acetylglucosamine (PNAG)-associated matrix biology.
CONCLUSIONS: Collectively, these data indicate that 2H-chromen-2-one is a promising antibiofilm adjuvant that can sensitize S. aureus biofilms to moxifloxacin, supporting its further validation in clinical isolates and in vivo models.
METHODS: Established biofilms were quantified by total biomass (crystal violet staining) and viable bacteria (CFU enumeration) following exposure to 2H-chromen-2-one alone or in combination with MXF, including testing MXF at a clinically relevant peak concentration (Cmax). Molecular docking was performed against proteins encoded by the ica locus to explore potential molecular targets.
RESULTS: 2H-chromen-2-one reduced biofilm biomass by approximately 50% at 1-2 mg/mL and markedly increased MXF antibiofilm killing in a concentration-dependent manner. Notably, MXF alone showed minimal killing at Cmax, whereas co-treatment achieved a reduction of up to approximately 1.6 log10 CFU/mL (>97% killing) and reduced the bactericidal concentration requirement from >1.5 to 0.032 mg/L. Moreover, the maximal reduction efficacy of MXF increased from approximately -2 log10 CFU/mL when MXF was used alone to approximately -3 log10 CFU/mL when combined with 2H-chromen-2-one. Docking suggested a putative interaction between 2H-chromen-2-one and IcaC, consistent with interference in poly-N-acetylglucosamine (PNAG)-associated matrix biology.
CONCLUSIONS: Collectively, these data indicate that 2H-chromen-2-one is a promising antibiofilm adjuvant that can sensitize S. aureus biofilms to moxifloxacin, supporting its further validation in clinical isolates and in vivo models.