Mitochondria Are a Subset of [EVs] Released by Activated Monocytes and Induce Type I IFN and TNF Responses in Endothelial Cells, 2019, Binder et al

Open access at https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.314601

 

Oh, very cool Andy.
Stuck in my foggy brain was the vague idea that chronic diseases other than ME have mitochrondrial dysfunction in affected cell types. Did not realize that there exists "microvesicle-embedded mitochondria"

This is from this Circ. Research article you posted above:

"What Is Known?

• Microvesicles, a subtype of extracellular vesicles, contribute to monocyte-endothelial cell signaling.
  
  
• Cargo and surface proteins are considered to define the inflammatory properties of microvesicles.
  
  
• Mitochondria are a source of damage-associated molecular patterns.
  
  
• Altered mitochondrial activity and cellular metabolism contribute to cardiovascular disease and other pathologies.
• 
  
• What New Information Does This Article Contribute?

• Lipopolysaccharide-activated monocytic cells release mitochondria and mitochondria embedded in microvesicles.
  
  
• Both free mitochondria and microvesicle-embedded mitochondria contribute to the ability of microvesicles to activate endothelial cells.
  
  
• This proinflammatory capacity is determined by the mitochondrial activity of parental cells rather than the mere presence of mitochondrial content.
  
  
• Mitochondria-associated TNF (tumor necrosis factor) and interferonogenic mitochondrial RNA are the major proinflammatory mediators of microvesicles released from activated monocytic cells."