Key Takeaways & Executive Findings
- •• • TFP2F achieved a 3-fold reduction in MIC80 from 7.5 μM (free TFP2) to 2.5 μM against drug-resistant P. aeruginosa under light irradiation, demonstrating enhanced targeting and phototoxicity. • • In a murine infected wound model, TFP2F plus light irradiation reduced wound area to <20% of initial by day 8, compared to >40% in controls, indicating accelerated healing. • • TFP2F eliminated >95% of P. aeruginosa within 2 days of treatment, showing rapid antibacterial efficacy critical for clinical infection control. • • TFP2 exhibited superior Type-I/II ROS generation, including hydroxyl radicals (·OH), superoxide (·O2−), and singlet oxygen (1O2), which are difficult for bacteria to develop resistance against.
Abstract
The escalating prevalence of multidrug-resistant Pseudomonas aeruginosa (P. aeruginosa) infections necessitates novel antibacterial strategies. Here, we engineered lectin B (LecB)-targeted glyco-dots (TFP2F) via self-assembly of a photosensitizer (TFP2) possessing aggregation-induced reactive oxygen species (ROS) generation capability with fucose-modified tetraphenylethene glycoclusters (TPE-Fuc4), enabling P. aeruginosa-targeted antimicrobial photodynamic therapy and wound healing promotion. Three photosensitizers (TFP0–2) featuring an “A-D-A” electronic structure were synthesized, exhibiting broad absorption bands and near-infrared (NIR) fluorescence. Among these, TFP2 demonstrated superior Type-I/II ROS production (including ·OH, ·O2−, and 1O2), achieving potent phototoxicity against P. aeruginosa (MIC80 = 7.5 μM). Self-assembly with TPE-Fuc4 yielded glyco-dots TFP2F that facilitated LecB-mediated bacterial targeting, enhanced bacterial uptake, and significantly reduced the MIC80 to 2.5 μM against drug-resistant P. aeruginosa under light irradiation. In a murine P. aeruginosa-infected wound model, TFP2F treatment combined with light irradiation accelerated wound closure to <20% of the initial area by day 8 (vs. >40% in controls) and eliminated >95% of bacteria by day 2. This work presents a convenient strategy for constructing glyco-dots as a potent functionalized platform for precision, lectin-targeted antimicrobial photodynamic therapy.
1. Introduction
Pseudomonas aeruginosa, a Gram-negative pathogen, accounts for at least 10% of acquired infections globally and is listed as a top-priority pathogen by WHO. Its ability to form biofilms—composed of eDNA, proteins, lectins, and exopolysaccharides—enhances antibiotic resistance and immune evasion, rendering conventional antibiotics increasingly ineffective. The rise of multidrug-resistant (MDR), extensively drug-resistant (XDR), and totally drug-resistant (TDR) strains underscores an urgent need for alternative antibacterial strategies that bypass traditional resistance mechanisms.
Antimicrobial photodynamic therapy (aPDT) offers a promising solution by generating cytotoxic reactive oxygen species (ROS) upon light activation, which non-specifically oxidize bacterial components, making resistance development unlikely. However, clinical translation is hampered by poor bacterial targeting and limited ROS generation in aggregated states. This study addresses these bottlenecks by engineering glyco-dots (TFP2F) that self-assemble from a photosensitizer (TFP2) with aggregation-induced ROS generation and fucose-modified tetraphenylethene glycoclusters (TPE-Fuc4). The fucose moieties specifically bind to LecB lectin on P. aeruginosa, enhancing bacterial uptake and local ROS concentration, thereby achieving potent antibacterial effects at low drug doses and promoting infected wound healing.
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DING Chenglong, XING Jing, DENG Yongpeng, WANG Yuli, XIE Jianjing, ZHANG Kexin, GONG Jin, LIU Jinyu, ZHANG Zhong, DONG Lei (2026). Tetraphenylethene-glycocluster camouflaged lectin B-targeted nano-photosensitizer for antimicrobial photodynamic therapy of Pseudomonas aeruginosa and infected wound healing. SCIENCE CHINA Materials. https://doi.org/10.1007/s40843-025-3979-3
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Frequently Asked Questions
What is the mechanism of enhanced targeting and how does it affect the MIC80 against drug-resistant P. aeruginosa?
The glyco-dots TFP2F are decorated with fucose moieties that specifically bind to LecB lectin on P. aeruginosa, facilitating targeted delivery and enhanced bacterial uptake. This targeting reduces the MIC80 from 7.5 μM (free TFP2) to 2.5 μM under light irradiation, indicating a 3-fold improvement in phototoxicity against drug-resistant strains.
How does TFP2F compare to conventional antibiotics in terms of resistance development?
TFP2F generates ROS through Type-I and Type-II pathways, including hydroxyl radicals, superoxide, and singlet oxygen. These ROS oxidize bacterial components non-specifically, making it difficult for bacteria to develop resistance, unlike conventional antibiotics that target specific pathways.
What are the in vivo outcomes of TFP2F treatment in infected wounds?
In a murine P. aeruginosa-infected wound model, TFP2F combined with light irradiation accelerated wound closure to <20% of the initial area by day 8, compared to >40% in controls. Additionally, it eliminated >95% of bacteria by day 2, demonstrating rapid and effective antibacterial activity.
What is the significance of the 'A-D-A' electronic structure in the photosensitizers?
The 'A-D-A' (acceptor-donor-acceptor) structure in TFP0–2 photosensitizers provides broad absorption bands and near-infrared fluorescence, which are beneficial for deep tissue penetration and efficient ROS generation. TFP2, with superior Type-I/II ROS production, was selected for further self-assembly.
How does the self-assembly with TPE-Fuc4 improve the photosensitizer's performance?
Self-assembly with TPE-Fuc4 forms glyco-dots TFP2F that exhibit aggregation-induced ROS generation, enhancing ROS production in the aggregated state. The fucose groups enable LecB-mediated targeting, increasing bacterial uptake and local ROS concentration, thereby reducing the effective dose and improving therapeutic efficacy.
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