Stiffness-Driven Modulation of Bactericidal Behavior in Nanostructured Polymer Thin Films

Abstract

The increasing use of medical implants, coupled with rising antimicrobial resistance, has intensified the need for effective antibacterial surface technologies. Protrusive nanostructured surfaces can mechanically disrupt bacterial membranes, leading to cell death, and have inspired extensive biomimetic design strategies. While prior studies have focused on the roles of nanostructure geometry, density, and surface chemistry, the intrinsic stiffness of nanostructured surfaces retaining same structures and chemistry remains poorly understood. Here, we systematically investigate the relationship between nanostructure stiffness and bactericidal efficacy by fabricating nanostructured polymer surfaces with tunable Young's moduli. Using Escherichia coli and Staphylococcus aureus as model Gram-negative and Gram-positive bacteria, respectively, we demonstrate that bactericidal efficacy against E. coli decreases with reduced nanostructure stiffness, consistent with diminished membrane tension. In contrast, S. aureus exhibits lower sensitivity to stiffness changes at higher moduli, reflecting its thicker and mechanically robust cell envelope. Notably, the softest nanopillars yield the highest bactericidal efficacy against S. aureus, attributed to enhanced nanopillar-cell interactions arising from bacterial cell geometry and increased structural deformability. Furthermore, highly deformable nanostructures promote additional bactericidal effects through lateral squeezing and cell sinking mechanisms. These findings reveal that bacterial cell size and morphology, in conjunction with nanostructure stiffness, critically govern bactericidal performance. This work provides mechanistic insight into stiffness-mediated bacterial membrane disruption and offers design principles for optimizing next-generation antibacterial surfaces.