由于异物反应和随后在植入物-组织界面1-4处形成纤维囊,植入的生物材料和设备长期面临功能和功效受损。在这里,我们证明了粘合剂植入物-组织界面可以减轻不同动物模型中的纤维囊形成。包括老鼠,老鼠,人源化小鼠和猪,与非粘附性植入物-组织界面相比,通过降低炎性细胞渗入粘附性植入物-组织界面的水平。组织学分析表明,粘合剂植入物-组织界面在不同器官上没有形成可观察到的纤维囊,包括腹壁,结肠,胃,肺和心脏,超过12周的体内。体外蛋白质吸附,多重Luminex检测,定量PCR,免疫荧光分析和RNA测序是额外进行验证的假设。我们进一步证明了在体内大鼠模型中通过具有粘合界面的可植入电极在12周内实现的长期双向电通信。这些发现可能为长期抗纤维化植入物-组织界面提供有希望的策略。
Implanted biomaterials and devices face compromised functionality and efficacy in the long term owing to foreign body reactions and subsequent formation of fibrous capsules at the implant-tissue interfaces1-4. Here we demonstrate that an adhesive implant-tissue interface can mitigate fibrous capsule formation in diverse animal models, including rats, mice, humanized mice and pigs, by reducing the level of infiltration of inflammatory cells into the adhesive implant-tissue interface compared to the non-adhesive implant-tissue interface. Histological analysis shows that the adhesive implant-tissue interface does not form observable fibrous capsules on diverse organs, including the abdominal wall, colon, stomach, lung and heart, over 12 weeks in vivo. In vitro protein adsorption, multiplex Luminex assays, quantitative PCR, immunofluorescence analysis and RNA sequencing are additionally carried out to validate the hypothesis. We further demonstrate long-term bidirectional electrical communication enabled by implantable electrodes with an adhesive interface over 12 weeks in a rat model in vivo. These findings may offer a promising strategy for long-term anti-fibrotic implant-tissue interfaces.