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Peer-reviewedCC BYRedox Biology

A ROS-responsive platelet extracellular vesicle biomimetic nanosystem regulates CD36/Fyn-CXCL-NETosis pathway-mediated immune-inflammatory amplification in the treatment of transfusion-related acute lung injury

  • Jiani Gao1
  • Ke Zhou2
  • Yijiu Ren1
  • Fengjing Yang3
  • Minjue Shan4
  • Yubing Fang4
  • Changbo Sun5
  • Weili Han6
  • Chang Chen7
  • Xuefei Hu5
7 affiliations
  1. 1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China
  2. 2Department of Lung Transplantation and Thoracic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China
  3. 3Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
  4. 4Tongji University School of Medicine, Shanghai, China
  5. 5Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China; Corresponding author. Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No. 507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
  6. 6Department of Lung Transplantation and Thoracic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China; Corresponding author. Department of Lung Transplantation and Thoracic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 1367, Wenyi West Road, Yuhang District, Hangzhou, 310003, Zhejiang Province, China.
  7. 7Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China; Clinical Center for Thoracic Surgery Research, Tongji University, Shanghai, China; Corresponding authors. Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, No. 507, Zhengmin Road, Yangpu District, Shanghai, 200433, China.
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Abstract

Transfusion-related acute lung injury (TRALI) remains a life-threatening complication of blood transfusion, yet the macrophage-neutrophil-NETosis inflammatory amplification mechanism and effective interventions are still incompletely defined. Here, we examined a CD36/Fyn-CXCL-related axis in TRALI and evaluated a ROS-responsive platelet extracellular vesicle biomimetic nanosystem (PEV@SP@EG) as a targeted delivery strategy. In a murine TRALI model, exploratory single-cell transcriptomic analysis showed immune-cell remodeling and linked CD36 expression to M1-like macrophage features. CD36 knockdown or pharmacological inhibition of Fyn/NF-kappaB reduced M1 polarization markers, CXCL production, and ROS generation. Conditioned medium from CD36-overexpressing BMDMs promoted neutrophil migration and NETosis, whereas CXCL-CXCR2 blockade or CD36/Fyn inhibition weakened these responses. PEV@SP@EG showed ROS-triggered drug release and preferential lung enrichment. In vivo , PEV@SP@EG attenuated CD36/Fyn-NF-kappaB-CXCL-related inflammatory signaling, NET formation, and oxidative stress in TRALI lung tissue, with concomitant improvement in lung architecture and gas exchange. These findings support a role for macrophage CD36/Fyn signaling in TRALI-associated macrophage-neutrophil inflammatory crosstalk and suggest that PEV@SP@EG may provide a targeted nanotherapeutic delivery platform for TRALI intervention.

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Cite

BibTeXRIS
BibTeX
@article{gao2026rosresponsive,
  title = {{A ROS-responsive platelet extracellular vesicle biomimetic nanosystem regulates CD36/Fyn-CXCL-NETosis pathway-mediated immune-inflammatory amplification in the treatment of transfusion-related acute lung injury}},
  author = {Jiani Gao and Ke Zhou and Yijiu Ren and Fengjing Yang and Minjue Shan and Yubing Fang and Changbo Sun and Weili Han and Chang Chen and Xuefei Hu},
  journal = {Redox Biology},
  year = {2026},
  month = oct,
  doi = {10.1016/j.redox.2026.104375},
  url = {https://doi.org/10.1016/j.redox.2026.104375},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - A ROS-responsive platelet extracellular vesicle biomimetic nanosystem regulates CD36/Fyn-CXCL-NETosis pathway-mediated immune-inflammatory amplification in the treatment of transfusion-related acute lung injury
AU  - Jiani Gao
AU  - Ke Zhou
AU  - Yijiu Ren
AU  - Fengjing Yang
AU  - Minjue Shan
AU  - Yubing Fang
AU  - Changbo Sun
AU  - Weili Han
AU  - Chang Chen
AU  - Xuefei Hu
PY  - 2026
DA  - 2026/10/30
JO  - Redox Biology
DO  - 10.1016/j.redox.2026.104375
UR  - https://doi.org/10.1016/j.redox.2026.104375
AB  - Transfusion-related acute lung injury (TRALI) remains a life-threatening complication of blood transfusion, yet the macrophage-neutrophil-NETosis inflammatory amplification mechanism and effective interventions are still incompletely defined. Here, we examined a CD36/Fyn-CXCL-related axis in TRALI and evaluated a ROS-responsive platelet extracellular vesicle biomimetic nanosystem (PEV@SP@EG) as a targeted delivery strategy. In a murine TRALI model, exploratory single-cell transcriptomic analysis showed immune-cell remodeling and linked CD36 expression to M1-like macrophage features. CD36 knockdown or pharmacological inhibition of Fyn/NF-kappaB reduced M1 polarization markers, CXCL production, and ROS generation. Conditioned medium from CD36-overexpressing BMDMs promoted neutrophil migration and NETosis, whereas CXCL-CXCR2 blockade or CD36/Fyn inhibition weakened these responses. PEV@SP@EG showed ROS-triggered drug release and preferential lung enrichment. In vivo , PEV@SP@EG attenuated CD36/Fyn-NF-kappaB-CXCL-related inflammatory signaling, NET formation, and oxidative stress in TRALI lung tissue, with concomitant improvement in lung architecture and gas exchange. These findings support a role for macrophage CD36/Fyn signaling in TRALI-associated macrophage-neutrophil inflammatory crosstalk and suggest that PEV@SP@EG may provide a targeted nanotherapeutic delivery platform for TRALI intervention.
SN  - 2213-2317
ER  -