Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor–α production in spleen by a mechanism requiring acetylcholine signaling through the alpha 7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells were required for the inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter acetylcholine required to control innate immune responses.
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Thursday, October 06, 2011
How our brain links to our immune system via vagus nerve
A large number of studies show that our psychological state can influence our immune system. Social isolation and stress weaken our immune system, and social affiliation and calm can strengthen it (the latter are associated with increased activity of the vagus nerve, which runs from the brainstem to many parts of the body). Now a multinational collaboration headed by Kevin Tracey has shown that stimulating the vagus nerve halts the pumping out of inflammatory signals by the immune system, with the neurotransmitter molecular responsible being acetyl choline - but, the Vagus nerve is not releasing it directly. Instead the splenic branch of the Vagus nerve is releasing noradrenaline in the spleen whose white blood cells (CD4 lymphocytes) are then secreting the acetyl choline which switches off production of inflammatory chemical by nearby cells. Here is the abstract:
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