Staphlyococcus epidermidis bacterial biofilm infections can develop at the vascular interface during intravenous catheter, infective endocarditis, and bloodstream infections. The primary virulence factor of S. epidermidis is biofilm formation. Bacterial biofilms are structured communities of bacterial cells encased within a self-produced extracellular matrix that are less susceptible to antibiotics and the host immune response than the planktonic phenotype. Previous studies of S. epidermidis with the vascular interface are limited to initial adhesion events of the bacteria to the vasculature and do not include biofilm development. Here we develop an in vitro model for evaluating S. epidermidis biofilm development at the vascular interface that enables live visualization of the vascular-biofilm interface during biofilm infection development. We report on the optimized coculture media required to sustain HUVEC morphology and viability as well as S. epidermidis biofilm development. Confocal laser scanning microscopy coupled with quantitative image analysis is used to quantify structural changes in biofilm development (biofilm thickness, biomass, surface area coverage) at the vascular interface as compared to monoculture biofilms. Additionally, changes in morphological features and the integrity of the HUVEC monolayer as a result of biofilm development at the interface are discussed. This work is an important step in advancing the understanding of S. epidermidis biofilm infection progression and recalcitrance at the vascular interface and has implications for the development of high-throughput testing of site-specific antibiofilm treatments.
