Topic: Extracellular Vesicle-Mediated Communication in the Gut–Liver–Brain Axis

The gut-liver-brain axis is a two-way communication system connecting the digestive tract, liver and the brain. This system modulates immune responses, metabolism and brain function both in health and disease. Alterations in the gut-liver-brain axis contribute to the neurological alterations in liver diseases and gastrointestinal disorders. For example, in liver cirrhosis, peripheral inflammation and hyperammonemia trigger neuroinflammation in the brain, leading to altered neurotransmission and neurological impairment. Similar mechanisms seem to be involved in the induction of cognitive impairment in patients with metabolic associated steatotic liver disease and bowel diseases. However, the mechanisms by which the peripheral alterations are transmitted to brain remain unclear. 

Extracellular vesicles (EV) seem to play an important role as messengers transmitting peripheral inflammatory, hepatic or gastrointestinal signals to the brain to induce neuroinflammatory responses and cognitive and motor impairment.  However, many details remain unknown concerning the pathologic effects of EV in these situations. For example: 
​● Which changes in the cargo of the EV are responsible for the transmission to brain of the deleterious effects?
● ​How does EV induce neuroinflammation in the brain?
​● Which cell types produce the pathologic EV?
● ​What triggers its production and the changes in the EV cargo?​
​● How can these changes be prevented to reverse the induction of cerebral alterations and neurological dysfunction?
​● May some component of the EV cargo serve as biomarker for liver or gastrointestinal disease state and/or for cognitive or motor impairment? 
● Do microbiota EV modulate the gut-liver-brain axis? 
● How peripheral inflammation influences the cargo and effects of EV?

This Special Issue on Extracellular Vesicle-Mediated Communication in the Gut-Liver-Brain axis welcomes articles providing advances in the above or related questions.