Silkworm excrement-derived carbon dots for sonodynamic bacterial killing and antioxidant-inflammatory modulation.

Persistent oxidative inflammation complicates the treatment of multidrug-resistant (MDR) bacterial infections. Sonodynamic therapy (SDT) enables ultrasound-activated bacterial killing but does not directly alleviate infection-associated oxidative stress. Here, phenylboronic acid (PBA)-functionalized carbon dots (PS-CDs) were prepared from silkworm excrement extract and PBA-terminated poly(ethylene glycol) (PBA-PEG-PBA) through a one-pot hydrothermal process. The PS-CDs showed spectroscopic features consistent with partially retained chlorophyll-derived chromophores, while PBA-PEG-derived groups improved aqueous dispersion and promoted bacterial association. Under ultrasound irradiation, PS-CDs generated reactive oxygen species (ROS) and reduced viable MDR Pseudomonas aeruginosa by 4.81 log10, accompanied by deoxyribonucleic acid and protein leakage. In the absence of ultrasound, PS-CDs scavenged 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radical cations (ABTS˙+), 2,2-diphenyl-1-picrylhydrazyl radicals (DPPH˙), and superoxide anions in concentration- and time-dependent manners. In lipopolysaccharide-stimulated RAW264.7 macrophages, PS-CDs reduced intracellular ROS and shifted CD86/CD206 expression toward an anti-inflammatory phenotype, with CD206-associated fluorescence accounting for 91.4% of the combined CD86/CD206 signal. Enzyme-linked immunosorbent assays further showed partial reductions in tumor necrosis factor-α, interleukin-6, and interleukin-1β secretion, together with increased transforming growth factor-β secretion. These findings provide an in vitro proof of concept for integrating ultrasound-activated bacterial killing with antioxidant and inflammatory modulation in a biomass-derived carbon dot platform.