Stimulation of nicotinic acetylcholine receptors (nAChRs), which are found on both nerves and immune cells, can initiate a program that shuts down the inflammatory machinery of immune cells, according to a paper in the August issue of Nature Immunology.
Such a trigger can be exploited to prevent inflammation. This new work adds to accumulating evidence that suggests the nervous system is intimately linked to the immune system.
Macrophages are immune cells that produce large amounts of proteins and chemicals to produce inflammatory effects. Wouter de Jonge and colleagues find that triggering nAChRs on macrophages sets off certain small molecules known as Jak2 and STAT3 in the cells to reduce inflammation by decreasing the production of offending proteins. To demonstrate the usefulness of this finding, they stimulate a major nerve (the vagus nerve) that links the brain to the gut in a mouse experiment that imitates inflammation after intestinal surgery. Normally, intestinal surgery can induce severe inflammation that leads to a condition known as postoperative ileus, which causes patients to suffer pain, nausea and vomiting. However, stimulation of the nerve, which specifically works through nAChR and STAT3, prevents inflammation of the intestine after surgery. Hence, therapies aimed at tickling nerves might provide new clinical avenues to treat postoperative ileus and other inflammatory conditions.
Wouter de Jonge (Academic Medical Center, Amsterdam, The Netherlands)
Additional contacts for comments:
Kevin J. Tracey (North Shore - Long Island Jewish Health System, Manhasset, NY, USA)
Christine N. Metz (The Picower Institute for Medical Research, Manhasset, NY, USA)
Also published online.
(C) Nature Immunology press release.
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