WASHINGTON (dpa-AFX) - Scientists at UC San Francisco have discovered how the gut sends signals to the brain to reduce appetite during a parasitic infection, showing that the immune system can actively make you feel less hungry.
During the study, the researchers focused on two rare types of cells in the gut. One type, called tuft cells, can detect parasites and start the body's immune response. Meanwhile, the other type, called enterochromaffin (EC) cells, sends signals to the brain by activating nearby nerve fibers. These EC cells are already known to cause feelings like nausea, pain, and stomach discomfort, but it was not clear if they interacted with tuft cells.
To study this, researcher Koki Tohara set up an experiment using special sensor cells placed next to tuft cells. When the tuft cells were exposed to a chemical called succinate, produced by parasitic worms, the sensor cells lit up. This showed that tuft cells were releasing acetylcholine, a chemical usually used by nerve cells to send messages.
The researchers then added acetylcholine to lab-grown gut tissue containing EC cells. The EC cells responded by releasing serotonin, a chemical that helps send signals through the vagus nerve from the gut to the brain.
'What we found is that tuft cells are doing something neurons do, but by a completely different mechanism,' Tohara said. 'They're using acetylcholine to communicate, but without any of the usual cellular machinery that neurons rely on to release it.'
The study also found that tuft cells release acetylcholine in two phases, which explains why people don't lose their appetite immediately after infection. At first, the release is small and short. Later, as the immune response becomes stronger, the number of tuft cells increases. This leads to a steady and stronger release of acetylcholine, which activates EC cells and sends signals to the brain to reduce appetite.
'This explains why you feel fine at first but then start to feel sick as the infection becomes established,' co-senior author David Julius said. 'The gut is essentially waiting to confirm that the threat is real and persistent before it tells the brain to change your behavior.'
To confirm this, the team studied mice with parasitic infections. Normal mice ate less as the infection progressed. However, mice that were modified so their tuft cells could not produce acetylcholine kept eating normally. This proved that this signaling pathway directly controls appetite.
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