Published online Jan 16, 2023. doi: 10.12998/wjcc.v11.i2.342
Peer-review started: November 5, 2022
First decision: November 22, 2022
Revised: December 3, 2022
Accepted: December 23, 2022
Article in press: December 23, 2022
Published online: January 16, 2023
Processing time: 67 Days and 23.2 Hours
Sepsis is a life-threatening complication of infection that involves endothelial injury that contributes to multiple organ failure. Microvesicles (MVs), which can transfer nucleic acids, organelles and proteins to target cells, are recognized as important mediators in intercellular communication.
MVs carrying mitochondrial content (mitoMVs) have been implicated in several diseases. However, it is not clear whether mitoMVs are involved in sepsis.
To explore whether mitoMVs constitute a subset of MVs isolated from plasma of patients with sepsis and contribute to endothelial activation.
Confocal microscopy and flow cytometry were used to characterize the presence of mitoMVs and their expression in plasma. Human umbilical vein endothelial cells were stimulated with circulating MVs to evaluate their effect on endothelial activation.
MVs isolated from patients with sepsis were rich in mitochondrial content and the levels of MVs and mitoMVs were significantly higher in patients with sepsis than in healthy controls. The number of mitoMVs was positively associated with tumour necrosis factor-α and soluble vascular cell adhesion molecule 1. MitoMVs isolated from the plasma of patients with sepsis induced elevated expression of type-I-IFN-dependent genes in endothelial cells.
MitoMVs were increased in the plasma of patients with sepsis and may activate the type I IFN signalling pathway in endothelial cells.
MitoMVs may have potential as a novel interventional target for sepsis-induced endothelial injury.