Overview
- UCSF-led researchers, whose peer-reviewed paper appeared Wednesday in Nature, traced a pathway from tuft cells to enterochromaffin cells to vagal nerves that lowers food intake.
- Tuft cells sensed parasite-made metabolites such as succinate and released acetylcholine, which prompted nearby enterochromaffin cells to secrete serotonin that activates the vagus nerve.
- The team found two acetylcholine phases from tuft cells, with an early burst followed by a sustained trickle that explains why appetite loss often appears days into infection.
- In mouse tests, infected animals ate less when tuft-cell acetylcholine signaling was intact, while engineered mice without that machinery kept eating, confirming the pathway drives the behavior.
- Tuft cells released acetylcholine without the usual neuronal release gear, revealing a non-neuronal route for gut–brain signaling that researchers say could inform future care for IBS and food intolerances.