Here's a couple of articles discussing how fat stimulates the vagus nerve and reduces inflammation.
http://www.medicalnewstoday.com/articles/31846.php
This one expands on the above:
http://jem.rupress.org/content/202/8/1014.1.full
http://jem.rupress.org/content/202/8/1023.full
Abstract (full paper at the above link)
http://www.medicalnewstoday.com/articles/31846.php
"Take two cheeseburgers and call me in the morning," may sound like far-fetched medical advice. After all, high fat foods can worsen blockages in blood vessels. But a new study in the October 17 issue of The Journal of Experimental Medicine shows that high fat foods can, at least in the gut, soothe inflammation. This action may stop immune cells from attacking food as a foreign invader.
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.
Nickey Henry
henryn@rockefeller.edu
212-327-8366
This one expands on the above:
http://jem.rupress.org/content/202/8/1014.1.full
Journal of Experimental Medicine
A study on page 1023 reveals a potential benefit of much-maligned high fat foods. According to Luyer and colleagues, the same hormone that makes you feel full after a fatty meal might also prevent immune cells from mistakenly attacking food proteins as if they were foreign invaders.Eating—particularly eating fat-rich foods—triggers the production of a hormone called cholecystokinin (CCK) by cells that line the small intestine. CCK binds to its receptor on cells in the gut, pancreas, and central nervous system (CNS), thus stimulating digestive functions, including gut peristalsis and insulin release, and triggering satiation. Luyer and his colleagues recently showed that dietary fat also blunts the inflammatory response in a rat model of hemorrhagic shock.
The new study connects CCK to a recently identified antiinflammatory pathway that is controlled by the vagus nerve. This pathway—dubbed the cholinergic antiinflammatory pathway—is mediated by the neurotransmitter acetylcholine, which is released from vagus nerve endings upon stimulation. Acetylcholine binds to nicotinic receptors on macrophages, thus inhibiting the synthesis and release of inflammatory cytokines such as TNF and interleukin (IL)-6.
Luyer et al. now show that the antiinflammatory effect of fat consumption in the rat model of hemorrhagic shock requires both CCK and the vagus nerve, as blocking CCK or severing the vagus nerve abolished this effect. With the vagus nerve intact, fat-induced CCK inhibited the production of circulating TNF and IL-6 and reduced gut permeability. Blocking nicotinic receptors also eliminated the antiinflammatory effects of dietary fat, thus solidifying the connection between fat-induced CCK and the cholinergic antiinflammatory pathway.
The authors think that this pathway might be important in suppressing gut inflammation in response to food proteins and normal gut bacteria, which immune cells might otherwise regard as foreign invaders. They also suggest that this pathway could potentially be targeted in patients as a way to reduce inflammatory complications after surgery.
http://jem.rupress.org/content/202/8/1023.full
Abstract (full paper at the above link)
The immune system in vertebrates senses exogenous and endogenous danger signals by way of complex cellular and humoral processes, and responds with an inflammatory reaction to combat putative attacks. A strong protective immunity is imperative to prevent invasion of pathogens; however, equivalent responses to commensal flora and dietary components in the intestine have to be avoided. The autonomic nervous system plays an important role in sensing luminal contents in the gut by way of hard-wired connections and chemical messengers, such as cholecystokinin (CCK). Here, we report that ingestion of dietary fat stimulates CCK receptors, and leads to attenuation of the inflammatory response by way of the efferent vagus nerve and nicotinic receptors. Vagotomy and administration of antagonists for CCK and nicotinic receptors significantly blunted the inhibitory effect of high-fat enteral nutrition on hemorrhagic shock-induced tumor necrosis factor-α and interleukin-6 release (P < 0.05). Furthermore, the protective effect of high-fat enteral nutrition on inflammation-induced intestinal permeability was abrogated by vagotomy and administration of antagonists for CCK and nicotinic receptors. These data reveal a novel neuroimmunologic pathway, controlled by nutrition, that may help to explain the intestinal hyporesponsiveness to dietary antigens, and shed new light on the functionality of nutrition.