The modification of polymer surfaces to mimic the extracellular matrix, and therefore, stimulate cell growth via receptor-mediated interactions, is one approach used to promote the integration of tissue-engineering scaffolds and biomaterials into the body. However, by optimizing surfaces for tissue integration it is likely that bacterial adhesion may also be affected, resulting in a greater risk of biomaterial-related infection. This could be detrimental to both the implant and the patient because biomaterial related infections are particularly resistant to host defenses and antibiotics. In this study, we analyzed the adhesion of a Staphylococcus epidermidis clinical isolate and 3T3 rat fibroblasts to tissue culture plastic coated with varying concentrations of fibronectin (Fn). Bacterial adhesion was always lower than tissue culture plastic and appeared to decrease with increasing Fn concentrations. Mammalian cell adhesion to Fn exceeded adhesion to tissue culture plastic but did not differ significantly over the range of protein concentrations or between 1 and 4 h of incubation. In most cases, the total surface coverage did not vary with time or Fn concentration, indicating that maximal cell adhesion and spreading occurred rapidly and at low protein concentrations. This study suggests that, by controlling the density of proteins or ligands on a surface, we can potentially optimize mammalian cell adhesion without stimulating bacterial adhesion, hence reducing the likelihood of infection.
Copyright 2001 John Wiley & Sons, Inc. J Biomed Mater Res 56: 222-227, 2001