Surface Engineering for Endothelium‐Mimicking Functions to Combat Infection and Thrombosis in Extracorporeal Life Support Technologies

• Published in: Advanced healthcare materials 2024-09, Vol.13 (22), p.e2400492-n/a
• Main Authors: Ashcraft, Morgan, Garren, Mark, Lautner‐Csorba, Orsolya, Pinon, Vicente, Wu, Yi, Crowley, Dagney, Hill, Joseph, Morales, Yeniselis, Bartlett, Robert, Brisbois, Elizabeth J., Handa, Hitesh
• Format: Article
• Language: English
• Subjects: Animals; antifouling; antimicrobial; Bacterial Adhesion; Biofouling; Biofouling - prevention & control; Blood; Blood circulation; Blood coagulation; Blood platelets; Blood Platelets - metabolism; Cell activation; Cell surface; Clotting; Endothelium; Endothelium - metabolism; hemocompatible; Homeostasis; Humans; In vivo methods and tests; Infections; Leukocytes; Medical equipment; Mimicry; Nitric oxide; Nitric Oxide - metabolism; Platelet Adhesiveness; Platelets; Polyethylene glycol; Polyethylene Glycols - chemistry; Protein adsorption; Robust control; Surface Properties; Thrombosis
• ISSN: 2192-2640; 2192-2659; 2192-2659
• DOI: 10.1002/adhm.202400492

Blood‐contacting medical devices routinely fail from the cascading effects of biofouling toward infection and thrombosis. Nitric oxide (NO) is an integral part of endothelial homeostasis, maintaining platelet quiescence and facilitating oxidative/nitrosative stress against pathogens. Recently, it is shown that the surface evolution of NO can mediate cell‐surface interactions. However, this technique alone cannot prevent the biofouling inherent in device failure with dynamic blood‐contacting applications. This work proposes an endothelium‐mimicking surface design pairing controlled NO release with an inherently antifouling polyethylene glycol interface (NO+PEG). This simple, robust, and scalable platform develops surface‐localized NO availability with surface hydration, leading to a significant reduction in protein adsorption as well as bacteria/platelet adhesion. Further in vivo thrombogenicity studies show a decrease in thrombus formation on NO+PEG interfaces, with preservation of circulating platelet and white blood cell counts, maintenance of activated clotting time, and reduced coagulation cascade activation. It is anticipated that this bio‐inspired surface design will enable a facile alternative to existing surface technologies to address clinical manifestations of infection and thrombosis in dynamic blood‐contacting environments. Vascular devices routinely fail due to surface‐induced thrombosis and infection. Nitric oxide (NO) is a promising agent to prevent platelet activation and microbial growth but cannot prevent any underlying protein surface fouling. A hierarchical strategy of controlled NO release with hydrophilic polyethylene glycol polymer interfaces is described for improved hemocompatibility and device patency in dynamic blood‐contacting applications.