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Cysteine Metabolism Reprogramming-Motivated Catalytic Immunotherapy for Orthopedic Biofilm Infections
Wanbo Zhu1, Min Ge2, Quan Liu3
1Department of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai 200233, P. R. China.
ACS Nano
|November 4, 2025
Summary
This study introduces a nanointerfering catalyst (niCatalyst) that reprograms cysteine metabolism to combat drug-resistant biofilm infections. The niCatalyst enhances immune responses, offering a novel metabolic immunotherapy approach for postantibiotic challenges.
Area of Science:
- Biomedical Engineering
- Immunology
- Microbiology
Background:
- Drug-resistant infections, particularly those involving medical implants, are challenging due to bacterial biofilms and immune suppression.
- Existing immunotherapies face limitations in overcoming biofilm defense mechanisms and the immunosuppressive biofilm-immune microenvironment (BIME).
Purpose of the Study:
- To develop a novel nanointerfering catalyst (niCatalyst) for targeted modulation of cysteine metabolism within the BIME.
- To investigate the potential of niCatalysts in enhancing antimicrobial immune responses and eliminating drug-resistant biofilm infections.
Main Methods:
- Development of a nanointerfering catalyst (niCatalyst) releasing aurin tricarboxylic acid to block cysteine metabolism enzymes.
- Utilizing light-triggered singlet oxygen catalysis to induce oxidative stress within biofilms.
- Assessing the impact of modulated cysteine metabolism on immune cell functions (macrophages, T cells, NK cells).
Main Results:
- The niCatalyst effectively limited hydrogen sulfide and glutathione production in biofilms by blocking cysteine metabolism.
- Light-triggered singlet oxygen catalysis increased oxidative damage within the biofilm.
- Interference with cysteine metabolism boosted macrophage antigen-presenting functions and costimulated antibiofilm adaptive T cells and NK cells.
- Successful elimination of drug-resistant biofilm infections with low metabolic activity was achieved.
Conclusions:
- Nanointerfering catalysts can reprogram cysteine metabolism in the biofilm-immune microenvironment.
- This approach effectively costimulates innate and adaptive immunotherapies against biofilms.
- Metabolic immunotherapy using niCatalysts presents a promising alternative for treating drug-resistant biofilm infections in the postantibiotic era.
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