Single-walled carbon nanotubes as a nano-weapons against biofilm of Pseudomonas aeruginosa

Background/introduction The emergence of antimicrobial resistance in bacterial biofilms represents a growing global healthcare burden, necessitating the development of novel agents with alternative mechanisms of action. Methods In the present study, we evaluated the antibacterial and antibiofilm potential of single-walled carbon nanotubes (SWCNTs) against Pseudomonas aeruginosa , a clinically significant opportunistic pathogen notorious for its robust biofilm-forming capacity and intrinsic resistance profile. Antimicrobial activity was assessed using disc diffusion and broth microdilution assays, while biofilm inhibition was quantified by crystal violet microplate assays. Scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy (FTIR) analyses were performed to elucidate the underlying antibacterial mechanism. Results SWCNTs exhibited potent concentration-dependent bacteriostatic and bactericidal effects, with a minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of 62.5 and 125 μg/mL, respectively. Zones of inhibition ranged from 14.5 ± 0.30 mm to 22.0 ± 0.57 mm across concentrations of 4–16 mg/mL ( p ≤ 0.05). In biofilm inhibition assays, planktonic growth (OD 470 ) was markedly reduced from ≈0.32 ± 0.01 in untreated controls to ≈0.05 ± 0.01 at 200 μg/mL, corresponding to a maximum biofilm inhibition rate of 85.5%. SEM imaging revealed pronounced morphological disruption of P. aeruginosa cell walls, including membrane deformation, surface roughening, and loss of cellular integrity upon SWCNT treatment, indicative of direct physical interaction between the nanotubes and bacterial membranes. FTIR analysis further corroborated these findings, demonstrating characteristic spectral shifts in functional groups associated with bacterial membrane lipids, proteins, and polysaccharides. Discussion/conclusion These spectral changes suggest physicochemical interactions that compromised membrane stability and disrupted biofilm matrix integrity. Collectively, these findings support a proposed mechanism whereby SWCNTs exert their antibacterial effect through direct membrane perturbation, interference with biofilm extracellular polymeric substances (EPS), and inhibition of early-stage biofilm adhesion and maturation.