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Counterselection against β-lactamase-expressing bacteria via an activatable photosensitizer that accumulates in resistant pathogens.

Created on 24 Jun 2026

Authors

Fangfang Chen, Yan Peng, Yifan Zhu, Hexin Xie

Published in

Proceedings of the National Academy of Sciences of the United States of America. Volume 123. Issue 26. Pages e2536405123. Jun 30, 2026. Epub Jun 23, 2026.

Abstract

The rapid global spread of antimicrobial resistance via β-lactamase (bla) demands targeted strategies that selectively eliminate resistant pathogens without exacerbating resistance. Herein, we report BIN-3I, a photosensitizer (PS) that enables bla-selective activation and-more importantly-covalent retention and accumulation within resistant bacteria, allowing potent photodynamic eradication of bla-expressing pathogens and exerting counter-selection pressure. BIN-3I adopts an enzyme-triggered "one-to-multi" design: Upon bla hydrolysis, it undergoes a hydrophilic-to-hydrophobic and low-to-high permeability transition, facilitating uptake and generating a reactive quinone methide intermediate that covalently binds intracellular proteins, leading to >2,000-fold accumulation within resistant bacteria, thiol depletion and light-triggered reactive oxygen species generation. In vitro, BIN-3I demonstrated bla-specific activation, selective enrichment in bla-expressing MRSA, and potent photodynamic killing (>99.999% reduction), outperforming the corresponding uncaged photosensitizer. Crucially, it selectively eradicates bla-producing MRSA within mixed populations, exerting counter-selection pressure against resistant strains. The PS also activates and accumulates in bla-expressing Gram-negative Enterobacter cloacae, albeit with reduced killing efficiency compared to Gram-positive bacteria. In vivo, it exhibited prolonged retention at infection sites and targeted imaging capability in murine myositis and abscess models. Notably, BIN-3I-mediated photodynamic therapy effectively cleared MRSA infections across multiple models-including thigh infection, wound, and biofilm-associated infections-achieving >5-log reduction in bacterial load and surpassing vancomycin in efficacy. This work presents a targeted antimicrobial platform that exploits bacterial resistance mechanisms to achieve species-specific eradication, offering a promising strategy to combat multidrug-resistant infections and alleviate the selection pressure that drives the enrichment of resistant strains.

PMID:
42335238
Bibliographic data and abstract were imported from PubMed on 24 Jun 2026.

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