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The role of extracellular vesicle fusion with target cells in triggering systemic inflammation

Author

Listed:
  • Praveen Papareddy

    (Lund University)

  • Ines Tapken

    (Lund University
    SMATHERIA gGmbH – Non-Profit Biomedical Research Institute
    Center for Systems Neuroscience (ZSN))

  • Keshia Kroh

    (Lund University
    Erasmus Medical Center)

  • Ravi Kiran Varma Bhongir

    (Lund University)

  • Milladur Rahman

    (Lund University)

  • Maria Baumgarten

    (Lund University)

  • Eda Irem Cim

    (Lund University)

  • Lilla Györffy

    (Lund University)

  • Emanuel Smeds

    (Lund University)

  • Ariane Neumann

    (Lund University)

  • Srinivas Veerla

    (Lund University)

  • Jon Olinder

    (Lund University)

  • Henrik Thorlacus

    (Lund University)

  • Cecilia Ryden

    (Lund University)

  • Eva Bartakova

    (Charles University and Military University Hospital Prague)

  • Michal Holub

    (Charles University and Military University Hospital Prague)

  • Heiko Herwald

    (Lund University)

Abstract

Extracellular vesicles (EVs) play a crucial role in intercellular communication by transferring bioactive molecules from donor to recipient cells. As a result, EV fusion leads to the modulation of cellular functions and has an impact on both physiological and pathological processes in the recipient cell. This study explores the impact of EV fusion on cellular responses to inflammatory signaling. Our findings reveal that fusion renders non-responsive cells susceptible to inflammatory signaling, as evidenced by increased NF-κB activation and the release of inflammatory mediators. Syntaxin-binding protein 1 is essential for the merge and activation of intracellular signaling. Subsequent analysis show that EVs transfer their functionally active receptors to target cells, making them prone to an otherwise unresponsive state. EVs in complex with their agonist, require no further stimulation of the target cells to trigger mobilization of NF-κB. While receptor antagonists were unable to inhibit NF-κB activation, blocking of the fusion between EVs and their target cells with heparin mitigated inflammation in mice challenged with EVs.

Suggested Citation

  • Praveen Papareddy & Ines Tapken & Keshia Kroh & Ravi Kiran Varma Bhongir & Milladur Rahman & Maria Baumgarten & Eda Irem Cim & Lilla Györffy & Emanuel Smeds & Ariane Neumann & Srinivas Veerla & Jon Ol, 2024. "The role of extracellular vesicle fusion with target cells in triggering systemic inflammation," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45125-1
    DOI: 10.1038/s41467-024-45125-1
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    References listed on IDEAS

    as
    1. Chong Shen & Shailendra S. Rathore & Haijia Yu & Daniel R. Gulbranson & Rui Hua & Chen Zhang & Nathan E. Schoppa & Jingshi Shen, 2015. "The trans-SNARE-regulating function of Munc18-1 is essential to synaptic exocytosis," Nature Communications, Nature, vol. 6(1), pages 1-10, December.
    2. Peter J. Wen & Staffan Grenklo & Gianvito Arpino & Xinyu Tan & Hsien-Shun Liao & Johanna Heureaux & Shi-Yong Peng & Hsueh-Cheng Chiang & Edaeni Hamid & Wei-Dong Zhao & Wonchul Shin & Tuomas Näreoja & , 2016. "Actin dynamics provides membrane tension to merge fusing vesicles into the plasma membrane," Nature Communications, Nature, vol. 7(1), pages 1-14, November.
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