Combatting biofilm formation of Klebsiella pneumoniae and Bacillus subtilis clinical strains from the oral cavity using biogenic Se-NPs: molecular docking simulation and cytotoxic effects on HepG2 cancer cells

Abstract

Abstract Bacterial biofilms are one of the primary causes of pathogenic activity in the oral environment; they adhere to both natural and artificial oral surfaces, causing cariogenic processes that result in dental decay and significantly reducing the lifespan of dental restoratives and prostheses; they can also affect the tissues surrounding teeth, causing gingival inflammation; persistent biofilms can cause damage to the alveolar bone, which in extreme cases may result in tooth loss; our study aims to isolate clinical isolates that are resistant to multiple drugs, before disarming them by suppressing the formation of biofilms. Klebsiella pneumoniae A11( K . pneumonia e) and Bacillus subtilis A33 ( B. subtilis ) clinical isolates were determined, and the most potent clinical isolates were identified as the most virulent strains for further investigations using 16 S rDNA PCR sequencing, with accession numbers PP995146 and PP995148 respectively. Synthesized selenium nanoparticles (Se-NPs) were analyzed using FTIR Spectroscopy, UV-Vis Spectroscopy, zeta potential, dynamic light scattering (DLS), X-ray diffraction (XRD), energy-dispersive X-ray analysis (EDX) of the [Se-NPs] solution revealed that it contained 88.49% selenium and 11.51% carbon, scanning electron microscopy (SEM), and transmission electron microscopy (TEM). According to TEM images, the average size of Se-NPs was 45.4 nm, and their shape was nearly spherical. The minimum inhibitory concentration (MICs) of biogenic Se-NPs were 0.25 mg/mL for K. pneumoniae A11 and 0.125 mg/mL for B. subtilis A33, with inhibition zones of 11–14 mm. Se-NPs significantly reduced biofilm formation at 0.125 and 0.25 mg/mL ( p < 0.05), by 85.08% in K. pneumoniae A11 and 75.45% in B. subtilis A33. A synergistic effect with azithromycin was observed, with fractional inhibitory concentration (FIC) values of 0.502 and 0.253, respectively. Molecular interactions showed Se-NPs forming hydrophobic contacts in K. pneumoniae LuxS Synthase (Asp52, Asp132; binding energy − 3.9020 kcal/mol) and B. subtilis AbbA (His3, Met4, Arg5; -4.2489 kcal/mol). Se-NPs had an IC 50 of 2.12 ± 0.02 µg/mL on HepG2 cells.