Eating -- particularly eating fat-rich foods -- causes cells in the small intestine to produce a hormone called cholecystokinin, or CCK. CCK stimulates digestion and gut peristalsis (the motion that propels food along the digestive tract), and also triggers satiation -- the full feeling that prompts you to stop eating.
The study by Luyer and colleagues shows that fat-induced CCK can also dampen inflammation in the gut, as rats fed a high-fat diet were protected against lethal bacteria-induced shock whereas those fed a low-fat diet were not. CCK sent signals to the brain through the vagus nerve, the nerve that provides the electrical regulation for many internal organs, including the gut and the heart. In response to CCK, vagus nerve endings in the gut released a neurotransmitter called acetylcholine. Acetylcholine then bound to proteins on immune cells and turned the cells off.
The authors think this pathway might explain why the immune system doesn't react to food proteins and normal gut bacteria as if they were foreign invaders. They also suggest that triggering this fat-driven chain of events in patients might provide a way to reduce inflammatory complications after surgery.