苯硼酸
免疫系统
炎症
透明质酸
伤口愈合
金黄色葡萄球菌
微生物学
细菌
硼酸
免疫学
抗菌剂
耐火材料(行星科学)
组织重塑
化学
药理学
内生
癌症研究
生物相容性材料
医学
生物
先天免疫系统
材料科学
免疫抑制
细胞生物学
慢性伤口
糖尿病
再生医学
脂磷壁酸
儿茶酚
细胞毒性
自愈水凝胶
葡萄球菌感染
作者
Yulong Lan,Xiaoliang Qi,J P Chen,Lifeng Tan,Jianliang Shen
摘要
ABSTRACT Methicillin‐resistant Staphylococcus aureus (MRSA)‐infected diabetic foot ulcers (DFUs) remain refractory to healing owing to persistent inflammation, hyperglycemia, and impaired tissue regeneration. Current antimicrobial strategies primarily eliminate viable bacteria but overlook pathogen‐associated molecular patterns (PAMPs) released upon bacterial death, which sustain NF‐κB/NLRP3 activation and prevent immune resolution. However, suppressing microbial burden without neutralizing PAMP‐driven inflammation fails to restore the regenerative wound microenvironment. Here, we report a self‐cascading hypoglycemic immunomodulatory hydrogel integrating Fe 3 O 4 @Au nanozymes with phenylboronic acid‐modified hyaluronic acid and dopamine‐functionalized silk fibroin. The platform exploits endogenous glucose to drive cascade catalysis for efficient MRSA eradication (∼99.99% with near‐infrared assistance), while dynamically exposing catechol and boronic acid motifs to sequester PAMPs and suppress inflammatory signaling. Consequently, macrophages are reprogrammed from pro‐inflammatory M1 to pro‐healing M2 phenotypes, enabling immune microenvironment remodeling. In MRSA‐infected DFU models, this coordinated antibacterial‐immunomodulatory strategy markedly accelerates wound closure, leaving only ∼13.97% residual area after 14 days. These results establish a design paradigm that couples biocatalysis with immune regulation for treating complex infected wounds.
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