Surfaces of implantable biomedical devices are increasingly engineered to promote their interactions with tissue. However, surfaces that stimulate desirable mammalian cell adhesion, spreading, and proliferation also enable microbial colonization. The biomaterials-associated infection that can result is now a critical clinical problem. We have identifi ed an important mechanism to create a surface that can simultaneously promote healing while reducing the probability of infection. Surfaces are created with submicrometer-sized, non-adhesive microgels patterned on an otherwise cell-adhesive surface. Quantitative force measurements between a staphylococcus and a patterned surface show that the adhesion strength decreases signifi cantly at inter-gel spacings comparable to bacterial dimensions. Time-resolved fl ow-chamber measurements show that the microbial deposition rate dramatically decreases at these same spacings. Importantly, the adhesion and spreading of osteoblast-like cells is preserved despite the sub-cellular non-adhesive surface features. Since such length-scale-mediated differential interactions do not rely on antibiotics, this mechanism can be particularly significant in mitigating biomaterials-associated infection by antibiotic-resistant bacteria such as MRSA.