Assessing the Therapeutic Potential of ZnO-NPs: Effects on Antibiotic Resistance and Biofilm Formation in Staphylococcus Aureus

Introduction: Staphylococcus aureus, known for its extensive genetic resistance elements and biofilm-forming capabilities, poses a significant challenge in clinical settings. This study aimed to investigate the prevalence of antibiotic resistance genes, the occurrence of biofilm formation genes, and the interrelation between zinc oxide nanoparticles (ZnO-NPs) and gene expression in S. aureus. Materials and Methods: Clinical isolates were procured from samples in Tehran, Iran, and identified through biochemical tests. Antibiotic susceptibility profiles were determined, and multidrug-resistant (MDR) strains were selected. The presence of resistance genes (vanA, mecA, and tetC) and biofilm formation genes (fnbA, fibA, clfA, and clfB) was assessed. Microdilution methods were employed to determine the minimum inhibitory concentration (MIC) using ZnO-NPs, and real-time PCR monitored the relationship between nanoparticle treatment and gene expression. Results: Results indicated high resistance among isolates to tetracycline (100%), amoxicillin (91%), ciprofloxacin, and oxacillin (85%), with low resistance to vancomycin (1%) and linezolid (2%). Profiling of resistance genes revealed a high prevalence of tetC (100%) and mecA (57%), while vanA exhibited a 0% prevalence. Biofilm formation genes were prevalent in 98% of strains, including clfA (98%), clfB (85%), fib (75%), and fnbA (0%). The MIC of iron oxide nanoparticles inhibiting S. aureus growth was recorded at 750 μg/mL. Real-time PCR results demonstrated a significant decrease in the expression of mecA (74%) and biofilm formation gene clfB (76%). Conclusion: This study underscores the potential efficacy of ZnO-NPs in mitigating bacterial resistance in both methicillin-resistant S. aureus (MRSA) and less-resistant strains (LRSA), impacting the expression of resistance and biofilm formation genes. The utilization of ZnO-NPs presents a promising strategy for managing MRSA/LRSA-associated diseases while minimizing antibiotic use.