| Summary: | The interaction between nanoplastics and bacteria remains still largely unclear. In this study, we determined the effect of nanopolystyrene particle (NP) on a bacterial pathogen of <i>Acinetobacter johnsonii</i> AC15. Scanning electron microscopy (SEM) analysis indicated the aggregation of NPs from 10 μg/L to 100 μg/L on surface of <i>A. johnsonii</i> AC15, suggesting that <i>A. johnsonii</i> AC15 acted as the vector for NPs. Exposure to 100–1000 μg/L NPs increased the growth and colony-forming unit (CFU) of <i>A. johnsonii</i> AC15. In addition, exposure to 100–1000 μg/L NPs enhanced the amount of formed biofilm of <i>A. johnsonii</i> AC15. Alterations in expressions of 3 survival-related (<i>zigA</i>, <i>basD</i>, and <i>zur</i>), 5 biofilm formation-related (<i>ompA</i>, <i>bap</i>, <i>adeG</i>, <i>csuC</i>, and <i>csuD</i>), and 3 serum resistance-related virulence genes (<i>lpxC</i>, <i>lpxL</i>, and <i>pbpG</i>) were observed after exposure to 1000 μg/L NPs. Moreover, both CFU and survival rate of <i>A. johnsonii</i> AC15 in normal human serum (NHS) were significantly increased by 1–1000 μg/L NPs, suggesting the enhancement in serum resistance of <i>Acinetobacter</i> pathogen by NPs. In the NHS, expressions of 3 survival-related (<i>zigA</i>, <i>basD</i>, and <i>zur</i>), 9 biofilm formation-related (<i>ompA</i>, <i>bap</i>, <i>adeF</i>, <i>adeG</i>, <i>csuA/B</i>, <i>csuC</i>, <i>csuD</i>, <i>csuE</i>, and <i>hlyD</i>), and 3 serum resistance-related virulence genes (<i>lpxC</i>, <i>lpxL</i>, and <i>pbpG</i>) were affected by 1000 μg/L NPs. Expressions of 1 survival-related (<i>zigA</i>), 5 biofilm formation-related (<i>bap</i>, <i>adeG</i>, <i>csuC</i>, <i>csuD</i>, and <i>csuE</i>), and 3 serum resistance-related virulence genes (<i>lpxC</i>, <i>lpxL</i>, and <i>pbpG</i>) were also altered by 10 μg/L NPs after the addition of NHS. Therefore, exposure to NPs in the range of μg/L has the potential to enhance bacterial virulence by increasing their growth, biofilm formation, and serum resistance.
|
|---|