article · Materials & Design
Chronic inflammatory conditions such as diabetic wounds suffer from continuous macrophage-driven inflammation that prevents proper tissue repair. To address this challenge, biomimetic polymeric particles inspired by apoptotic cell membranes have been engineered with an inflammation-responsive design. In these particles, phosphatidylserine is temporarily shielded by polyethylene glycol via an acid-sensitive chemical bond. In the acidic microenvironment typical of inflamed tissue, the protective layer detaches, exposing phosphatidylserine to enhance uptake by macrophages. Laboratory evaluations confirmed that the exposed particles suppress inflammatory signalling pathways, notably inhibiting NF-κB and interleukin-6, whilst reducing tumour necrosis factor-alpha and elevating transforming growth factor-beta-1. When tested in a diabetic wound model, the particles significantly accelerated wound closure, promoted collagen deposition, reduced granulation tissue, and supported histological healing compared to untreated wounds.
Diabetic wounds struggle to heal because persistent inflammation stalls normal tissue repair mechanisms. By mimicking natural clearance signals from dying cells exclusively within inflamed environments, this targeted approach dampens excessive immune responses locally. If developed further, such biomaterials could offer more precise treatments to restart regeneration in non-healing wounds without causing widespread immune disruption.
This technology could enable advanced topical formulations or smart dressings for chronic wounds and diabetic ulcers, targeting wound care clinicians and advanced wound care manufacturers. Having demonstrated efficacy in cellular assays and in an animal diabetic wound model, the technology sits at an applied research stage. Significant pre-clinical safety profiling, process scale-up, and human clinical testing will be required before commercial adoption.
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Chronic inflammatory disorders, particularly diabetic wounds, are characterized by persistent macrophage-mediated inflammation that delays tissue repair. Herein, we developed pH-responsive apoptotic cell membrane-inspired polymeric particles in which phosphatidylserine (PS) was temporarily shielded by polyethylene glycol (PEG) through an acid-labile Schiff base linkage to achieve inflammation-responsive activation. The PEG-PS particles were synthesized and characterized by NMR, GPC, DLS, and zeta potential measurements. Their pH-responsive behavior, macrophage uptake, and anti-inflammatory activity were evaluated in vitro, while therapeutic efficacy was assessed in a streptozotocin-induced diabetic wound model. Under acidic conditions, PEG shedding promoted PS exposure, resulting in enhanced macrophage uptake, significant inhibition of NF-κB activation and IL-6 production, together with reduced TNF-α and increased TGF-β1 expression. In vivo, PEG-PS particles significantly accelerated wound closure, reduced granulation tissue formation, enhanced collagen deposition, and improved histological healing compared with PS particles and untreated diabetic wounds. These findings demonstrate that pH-responsive PEG shielding provides controlled activation of PS-mediated immunomodulation and represents a promising strategy for inflammation regulation and diabetic wound healing.
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DOI: 10.1016/j.matdes.2026.116821
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