One of the main tasks of the immune system is to discriminate and appropriately react
to “danger” or “non-danger” signals. This is crucial in the gastrointestinal tract,
where the immune system is presented with a myriad of food antigens and symbiotic
microflora that are in constant contact with the mucosa, in addition to any potential
pathogens. This large number of antigens and symbionts are essential for providing
vital nutrients, must be tolerated by the intestinal immune system to prevent aberrant
inflammation. Hence, the balance between immune activation versus tolerance should be tightly regulated to maintain intestinal homoeostasis and to
prevent immune activation indiscriminately against all luminal antigens. Loss of this
delicate equilibrium can results in chronic activation of the intestinal immune response
resulting in intestinal disorders such as inflammatory bowel disease (IBD). Recent
evidence from our research group supports the idea that an additional actor, the vagus
nerve via the enteric nervous system may play a critical role in modulating the intestinal
microenvironment preserving immune homeostasis and tolerance. For the first time we
were able to show that activation of enteric neurons (ENs) via electrical stimulation
of vagus nerve or via specific chemical compounds, lowered intestinal inflammation,
reduced cytokines expression and decreased recruitment of inflammatory immune cells
in a murine model of postoperative ileus (Matteoli G, et al.; Gut. 2014 Jun;63(6):938–48).
This effect was dependent on resident macrophages expressing α7nAChR. Indeed, α7nAChR
activation reduces ATP-induced Ca2+ increase “in situ” in small intestine resident macrophages. Our present study suggests that intestinal
muscularis resident macrophages, modulated by neurotransmitters release by enteric
neurons, representing the ultimate target of the gastrointestinal cholinergic anti-inflammatory
pathway.
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© 2015 Published by Elsevier Inc.