文献类型：期刊文献

英文题名：O2-releasing microneedle platform eradicates drug-resistant bacterial biofilm via metabolic interference and innate immune reactivation

作者：Liu, Shangpeng[1];Zhang, Zhuo[1];Ge, Zhenghong[1];Teng, Runxing[1];Chen, Ran[1];Qin, Jinlong[2];Sun, Min[1,3];Du, Jianzhong[1,3];Fan, Zhen[1]

机构：[1]Tongji Univ, Sch Mat Sci & Engn, Dept Polymer Mat, Shanghai 201804, Peoples R China;[2]Tongji Univ, Shanghai Peoples Hosp 4, Sch Med, Dept Gynaecol & Obstet, Shanghai 200434, Peoples R China;[3]East China Univ Sci & Technol, Sch Mat Sci & Engn, Shanghai 200237, Peoples R China

年份：2026

卷号：335

外文期刊名：BIOMATERIALS

收录：;EI(收录号：20262320828581);WOS:【SCI-EXPANDED(收录号:WOS:001785568200001)】；

基金：This research was supported by National Key R & D Program of China (2024YFB4710300) , National Natural Science Foundation of China (22475154, 52573139, 22335005, and 22305177) , international scientific collaboration fund of Science and Technology Commission of Shanghai Municipality (23520710900) , Innovation Program of Shanghai Municipal Education Commission (2023ZKZD28) , Shanghai Hongkou District Public Health Key Support Discipline Construction Project (HKGWFC 202401) , and the Fundamental Research Funds for the Central Universities (501100012226) .

语种：英文

外文关键词：Ferroptosis-like death; Microneedle; Biofilm; Diabetic wound healing; Immune reactivation

摘要：Biofilm-associated infections pose formidable clinical challenges due to their complicated microenvironment characterized by dense extracellular polymeric substances (EPS), hypoxia, and excessive H2O2. While microneedles can mechanically penetrate biofilms, their efficacy is limited by poor diffusion of antibacterial agents through EPS and secondary infection resulting from escaping planktonic bacteria. Herein, we proposed an oxygen-powered microneedle (FeCN@MN) that synergistically eradicates biofilms through a dual mechanism: ferroptosis-like death-mediated bacterial killing and neutrophil reactivation. The microneedle utilizes sodium percarbonate (SPO) particles that react with interstitial fluid to generate O2 bubbles, which propel the loaded FeS2-decorated carbon nanospheres (FeCN) to disperse throughout biofilms. Moreover, the FeCN@MN can reactivate neutrophils to scavenge planktonic bacteria escaping from biofilm disintegration through enhanced chemotaxis and respiratory burst, further inhibiting potential recurrence of infection. In vitro experiment reveals that iron overload disrupts amino acid metabolism and peroxide accumulation, promoting bacterial ferroptosislike death. Furthermore, neutrophil functional tests show enhanced chemotaxis and killing ability to MRSA bacteria. In MRSA biofilm-infected diabetic wound model, FeCN@MN significantly dismantles biofilms, and effectively eliminates infections. In conclusion, this two-stage therapeutic approach combining bacterial metabolic interference with immune response reactivation provides a promising strategy in eradicating drug-resistant bacterial biofilm-associated infections.