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• NPs entered the intracellular region and caused plasmolysis and cytoplasm outflow. • NPs stimulated the initial cell attachment and aggravated NF membrane biofouling. • Low NPs exposure promoted cell secretion, quorum sensing and homologous recombination. • High NPs condition induced cell lysis, metabolic inactivation and genomic DNA damage. The release of nanoplastics (NPs) into the environment is growing due to the extensive use of plastic products. Numerous studies have confirmed the negative effects of NPs on microorganisms, which poses uncertainties concerning their impact on nanofiltration (NF) membrane biofouling. This study investigated the initial cell adhesion process, NF membrane biofouling kinetic processes and bacterial responses of Pseudomonas aeruginosa (P. aeruginosa) exposed to varied NPs concentrations (0–50 mg·L−1). Transcriptome analysis demonstrated that low concentration of NPs (0.1 mg·L−1) promoted bacterial quorum sensing, energy metabolism, exopolysaccharide biosynthesis and bacterial secretion systems. Correspondingly, the polysaccharide content increased remarkably to 2.77 times the unexposed control, which served as a protective barrier for bacteria to avoid the impact of NPs-induced stress. Suppressed homologous recombination, microbial metabolic potentials and flagellar assembly were detected in bacteria exposed to a high concentration (50 mg·L−1) of NPs, mainly due to the triggered reactive oxygen species (ROS) generation, genomic DNA damage, and decreased energy production. Overall, enhanced formation of the extracellular polymeric substances (EPS) and aggravated membrane flux decline were observed when NPs interacted with the membrane surface by cell secretions (low NPs levels) or cell lysis (high NPs levels). These findings shed light on understanding the microbial metabolism mechanism and membrane biofouling propensity with NPs stress at both the molecular and gene levels. [Display omitted] [ABSTRACT FROM AUTHOR]

• The impact of antibiotic resistance on initial bacterial adhesion and biofilm formation on plastics was explored. • Single-cell adhesion spectroscopy was used to probe the initial cell adhesion on plastics. • Antibiotic resistance promoted biofilm growth on plastics by enhancing initial bacterial adhesion in antibiotic environments. The microbial biofilm formed on plastics, is ubiquitous in the environment. However, the effects of antibiotic resistance on the development of the biofilm on plastics, especially with regard to initial cell attachment, remain unclear. In this study, we investigated the initial bacterial adhesion and subsequent biofilm growth of a rifampin (Rif) resistant E. coli (RRE) and a normal gram-positive B. subtilis on a typical plastic (polyethylene, PE). The experiments were conducted in different antibiotic solutions, including Rif, sulfamethoxazole (SMX), and kanamycin (KM), with concentrations ranging from 1 to 1000 μg/L to simulate different aquatic environments. The AFM-based single-cell adhesion force determination revealed that Rif resistance strengthened the adhesion force of RRE to PE in the environment rich in Rif rather than SMX and KM. The enhanced adhesion force may be due to the higher secretion of extracellular polymeric substances (EPS), particularly proteins, by RRE in the presence of Rif compared to the other two antibiotics. In addition, the higher ATP level of RRE would facilitate the initial adhesion and subsequent biofilm growth. Transcriptome analysis of RRE separately cultured in Rif and SMX environments demonstrated a clear correlation between the expression of Rif resistance and the augmented bacterial adhesion and cellular activity. Biofilm biomass analysis confirmed the promotion effect of Rif resistance on biofilm growth when compared to non-resistant biofilms, establishing a novel association with the augmentation of microbial adhesion force. Our study highlights concerns related to the dissemination of antibiotic resistance during microbial colonization on plastic that may arise from antibiotic resistance. [Display omitted] [ABSTRACT FROM AUTHOR]