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用于生物电子学的具有抑制异物反应的半导体聚合物的免疫兼容设计。

Immune-compatible designs of semiconducting polymers for bioelectronics with suppressed foreign-body response.

作者信息

Li Nan, Kang Seounghun, Liu Zhichang, Wai Shinya, Cheng Zhe, Dai Yahao, Solanki Ani, Li Songsong, Li Yang, Strzalka Joseph, White Michael J V, Kim Yun-Hi, Tian Bozhi, Hubbell Jeffrey A, Wang Sihong

机构信息

Pritzker School of Molecular Engineering, The University of Chicago, Chicago, IL, USA.

Department of Chemistry, The University of Chicago, Chicago, IL, USA.

出版信息

Nat Mater. 2025 Apr 17. doi: 10.1038/s41563-025-02213-x.

Abstract

One of the greatest obstacles to achieving implantable electronics with long-term functionality and minimized inflammatory reactions is the immune-mediated foreign-body response (FBR). Recently, semiconducting polymers with mixed electron-ion conductivity have been demonstrated as promising candidates to achieve direct electrical interfacing on bio-tissues. However, there is limited understanding of their immune compatibility in vivo, and strategies for minimizing the FBR through molecular design remain underexplored. Here we introduce a set of molecular design strategies for enhancing the immune compatibility of semiconducting polymers. Specifically, we show that selenophene, when incorporated in the backbone, can mitigate the FBR by suppressing macrophage activation. In addition, side-chain functionalization with immunomodulatory groups decreases the FBR further by downregulating the expression of inflammatory biomarkers. Together, our synthesized polymers achieve suppression of the FBR by as much as 68% (as indicated by the collagen density). In the meantime, these immune-compatible designs still provide a high charge-carrier mobility of around 1 cm V s. We anticipate that such immune-compatible design principles can be translated to a variety of conjugated polymers to suppress the FBR for implantable applications.

摘要

实现具有长期功能且炎症反应最小化的可植入电子设备的最大障碍之一是免疫介导的异物反应(FBR)。最近,具有混合电子-离子传导性的半导体聚合物已被证明是在生物组织上实现直接电接口的有前途的候选材料。然而,人们对它们在体内的免疫相容性了解有限,通过分子设计最小化FBR的策略仍未得到充分探索。在此,我们介绍了一组用于增强半导体聚合物免疫相容性的分子设计策略。具体而言,我们表明,当硒吩并入主链时,可以通过抑制巨噬细胞活化来减轻FBR。此外,用免疫调节基团进行侧链功能化可通过下调炎症生物标志物的表达进一步降低FBR。我们合成的聚合物共同实现了对FBR高达68%的抑制(以胶原蛋白密度表示)。与此同时,这些免疫相容性设计仍提供约1 cm V s的高载流子迁移率。我们预计,这种免疫相容性设计原则可应用于各种共轭聚合物,以抑制用于可植入应用的FBR。

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