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

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 Olinder, Henrik Thorlacus, Cecilia Ryden, Eva Bartakova, Michal Holub and Heiko Herwald ()
Additional contact information
Praveen Papareddy: Lund University
Ines Tapken: Lund University
Keshia Kroh: Lund University
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

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: 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.

Date: 2024
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45125-1

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DOI: 10.1038/s41467-024-45125-1

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