吉林大学杨英威团队报道了超分子开关激活的群体感应阱，用于病原体特异性识别和根除治疗肠炎。相关研究成果发表在2024年12月12日出版的《美国化学会杂志》。

肠道细菌感染已成为人类健康的重大威胁。然而，目前典型的基于抗生素的疗法不仅会导致耐药性，还会破坏肠道微生物群平衡，对生命活动产生额外的不利影响。迫切需要开发新的抗菌材料，在不破坏有益细菌群落或促进耐药性的情况下选择性地消除致病菌。

该文中，研究人员利用细菌群体感应（QS）这一调节群落行为的通用机制，通过将葫芦脲[7]uril（CB[7]）包封在1-乙烯基-3-戊基咪唑鎓溴化物（[VPIM]Br）上，通过主客体相互作用形成超分子开关（[VPIM]BrCB[7]，然后使用原子转移自由基聚合将其接枝到细菌细胞表面，从而开发出超分子QS陷阱。

随后，通过细菌间QS信号识别和聚集匹配的病原体。此外，添加金刚烷胺（AD）通过CB[7]与[VPIM]BrCB[7]的竞争性结合来促进[VPIM]Br的释放，以进行灭菌。这种QS陷阱专门触发匹配细菌的自聚集和有效消除。基于[VPIM]BrCB[7]的陷阱可以增加小鼠肠道微生物的多样性和丰度，有效治疗大肠杆菌K88诱导的肠道损伤，而不会扰乱肠道微生物群平衡。

这种超分子开关QS陷阱开辟了一条有前景的途径，可以专门识别和根除病原体，用于无抗生素治疗肠道细菌感染和其他炎症性疾病。

附：英文原文

Title: Supramolecular Switching-Enabled Quorum Sensing Trap for Pathogen-Specific Recognition and Eradication to Treat Enteritis

Author: Xiaojie Wu, Qinggele Borjihan, Yueying Su, Haoran Bai, Xinshang Hu, Xin Wang, Jing Kang, Alideertu Dong, Ying-Wei Yang

Issue&Volume: December 12, 2024

Abstract: Intestinal bacterial infections have become a significant threat to human health. However, the current typical antibiotic-based therapies not only contribute to drug resistance but also disrupt gut microbiota balance, resulting in additional adverse effects on life activities. There is an urgent need to develop new antibacterial materials that selectively eliminate pathogenic bacteria without disrupting beneficial bacterial communities or promoting drug resistance. Herein, we utilize bacterial quorum sensing (QS), a universal mechanism for regulating community behavior, to develop a supramolecular QS trap by encapsulating cucurbit[7]uril (CB[7]) on 1-vinyl-3-pentylimidazolium bromide ([VPIM]Br) to form a supramolecular switch ([VPIM]BrCB[7]) through host–guest interactions followed by grafting it onto bacterial cell surfaces using atom transfer radical polymerization. Subsequently, the matched pathogens are recognized and aggregated through interbacterial QS signals. Furthermore, the addition of amantadine (AD) facilitates the release of [VPIM]Br by competitive binding of CB[7] on [VPIM]BrCB[7] for sterilization. This QS trap specifically triggers the self-aggregation and efficient elimination of matched bacteria. The [VPIM]BrCB[7]-based trap can increase the diversity and abundance of intestinal microorganisms in mice, effectively treating Escherichia coli K88-induced intestinal damage without perturbing gut microbiota balance. This supramolecular-switched QS trap opens up a promising avenue to specifically recognize and eradicate pathogens for the antibiotic-free treatment of intestinal bacterial infections and other inflammatory diseases.

DOI: 10.1021/jacs.4c14424

Source: https://pubs.acs.org/doi/abs/10.1021/jacs.4c14424