Polystyrene nanoplastics and pathogen plasticity: Toxic threat or tolerated stressor in Salmonella enterica?

Polystyrene nanoplastics (PS-NPs), a group of increasingly common environmental pollutants, pose emerging risks to microbial ecology and food safety. This study examines the concentration- and time-dependent effects of PS-NPs (low exposure: 2.5-5 mg/L; moderate exposure: 10-20 mg/L; high exposure: 50-100 mg/L) on Salmonella enterica , a major foodborne pathogen. Under realistic environmental conditions, PS-NPs influenced bacterial viability, membrane integrity, and oxidative stress levels, with higher concentrations causing lipid peroxidation and membrane disruption. Gene expression analyses showed early upregulation of stress-related, biofilm-associated, virulence, and adhesion genes, indicating an adaptive response to PS-NP-induced stress. Biofilm formation increased with moderate to high PS-NP exposure, confirmed by exopolysaccharide measurement and confocal microscopy. However, prolonged or high-dose exposure resulted in downregulation of efflux systems ( acrB , tolC ), quorum-sensing regulators ( lsrA , invF ), and antimicrobial resistance genes ( marR , tetC ), suggesting stress-related trade-offs. Notably, transient activation of marA and acrA indicates potential NP-induced cross-resistance mechanisms. These results imply that PS-NPs act as environmental stressors capable of altering bacterial virulence and survival strategies, with significant implications for microbial behavior in plastic-contaminated ecosystems and food processing environments. Collectively, our results emphasize the urgent need to reevaluate NP exposure in the context of public health and antimicrobial resistance. • PS-NPs suppress Salmonella viability in a clear concentration-dependent manner. • Exposure to PS-NPs activates key oxidative and envelope stress response pathways. • PS-NPs enhance biofilm formation, promoting persistence under adverse conditions. • PS-NPs modulate virulence genes, influencing invasive and pathogenic potential. • PS-NPs alter AMR gene expression, influencing resistance dissemination.