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<p>Skin wounds are refractory due to antibiotic-resistant bacterial infection. Although the photodynamic therapy exerts superiority because of noninvasiveness, high efficiency and no drug resistance, the therapeutic effect is constrained by the complex structure of wound tissue and diffuse drug distribution. The proinflammatory cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) regulates tissue repair by engaging its receptor Fn14, which is highly expressed in wounds. In this study, we developed a novel photosensitizer, the selenoviologen-TWEAK conjugate (SeV-Tp), to enhance selective enrichment and synergistically promote wound healing. <i>In vitro</i> analyses demonstrated that SeV-Tp, under visible light, generated high levels of reactive oxygen species, resulting in potent antibacterial activity against both Gram-positive and Gram-negative bacteria. Notably, SeV-Tp selectively bound to Fn14 and amplified fibroblast activation via photodynamic cooperation. In a mouse model of antibiotic-resistant <i>Pseudomonas aeruginosa</i>-infected wound, SeV-Tp accelerated the healing by reducing bacterial burden, modulating the immune microenvironment, promoting collagen deposition, and stimulating hair follicle regeneration. Moreover, SeV-Tp preferentially accumulated within wound tissues with minimal adverse effects. SeV-Tp represents a strategy that selectively enriches and harnesses synergistic benefits from both components, positioning SeV-Tp as a promising photosensitizer for the treatment of refractory wounds.</p>

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TWEAK-conjugated selenoviologen as a novel photosensitizer for selective wound accumulation and synergistic healing of drug-resistant bacterial infections

  • 期刊论文

  • 发表日期：

    2026年3月13日

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  • Xiaoying Ning,
  • Qi Sun,
  • Yanfei Zhang,
  • Mai Luo,
  • Fan Bai,
  • Zhu Yan,
  • Yufei Zhang,
  • Chaim Putterman,
  • Gang He,
  • Yumin Xia

摘要

Skin wounds are refractory due to antibiotic-resistant bacterial infection. Although the photodynamic therapy exerts superiority because of noninvasiveness, high efficiency and no drug resistance, the therapeutic effect is constrained by the complex structure of wound tissue and diffuse drug distribution. The proinflammatory cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) regulates tissue repair by engaging its receptor Fn14, which is highly expressed in wounds. In this study, we developed a novel photosensitizer, the selenoviologen-TWEAK conjugate (SeV-Tp), to enhance selective enrichment and synergistically promote wound healing. In vitro analyses demonstrated that SeV-Tp, under visible light, generated high levels of reactive oxygen species, resulting in potent antibacterial activity against both Gram-positive and Gram-negative bacteria. Notably, SeV-Tp selectively bound to Fn14 and amplified fibroblast activation via photodynamic cooperation. In a mouse model of antibiotic-resistant Pseudomonas aeruginosa-infected wound, SeV-Tp accelerated the healing by reducing bacterial burden, modulating the immune microenvironment, promoting collagen deposition, and stimulating hair follicle regeneration. Moreover, SeV-Tp preferentially accumulated within wound tissues with minimal adverse effects. SeV-Tp represents a strategy that selectively enriches and harnesses synergistic benefits from both components, positioning SeV-Tp as a promising photosensitizer for the treatment of refractory wounds.