生物膜
TLR4型
细胞生物学
微生物学
TLR9型
免疫系统
先天免疫系统
化学
基因沉默
诱饵
糖尿病足
炎症
TLR2型
生物
免疫学
重编程
癌症研究
下调和上调
脂多糖
信号转导
体内
碎片(计算)
乳铁蛋白
血管生成
促炎细胞因子
细菌
慢性伤口
作者
Junfeng Song,Y Song,Xirui Huang,Xingjin Li,Lifei Gao,Y C Wang,Tianbao Zhu,Xiaomin Li,Shuai Wang,Tiancong Zhao,Dongyuan Zhao
摘要
ABSTRACT Chronic diabetic foot infections are severely hindered by tough biofilms and a self‐fueling hyperinflammatory microenvironment, primarily orchestrated by the synergistic interplay between extracellular DNA (eDNA) and lipopolysaccharides (LPS) which facilitates the assembly of impenetrable biofilm architectures while inducing cross‐inflammatory activation through the TLR4/9 axis. Conventional therapies often fail to resolve these “dual traps” of structural resistance and immunological interference. Herein, we developed a multifunctional mesoporous nano‐regulator composed of Colistin (CT) and m‐aminophenol formaldehyde (mAPF) framework, hence termed CT/mAPF to implement a “triad‐strategy”: biofilm disruption, bacterial eradication, and debris neutralization. The CT/mAPF nano‐regulator achieves potent bactericidal activity (99.99%) and initiates ROS‐mediated oxidative fragmentation of eDNA to destroy the biofilm scaffold. Crucially, the platform effectively neutralizes LPS and degrades eDNA, leading to the simultaneous silencing of TLR4 and TLR9 signaling pathways. This dual‐targeting approach weakens the eDNA/LPS‐mediated synergistic inflammatory response, and suppresses pro‐inflammatory cytokines ( IL‐6 , IL‐1β , TNF‐α ). In diabetic mouse models, CT/mAPF significantly accelerated bacterial clearance and wound closure through enhanced angiogenesis and collagen maturation. This integrated strategy resolves the cycle of chronic infection and inflammation, offering a robust strategy for Gram‐negative bacteria‐infected diabetic wound management.
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