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. 2017 Oct 18;8:1321. doi: 10.3389/fimmu.2017.01321

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Copyright © 2017 Tanaka, Arima, Kamimura and Murakami.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Inflammatory reflex. Afferent (1) and efferent vagus nerve (2) stimulation by systemic pro-inflammatory cytokines and/or pathogen-associated molecular patterns (PAMPs) during septic shock, ischemia–reperfusion injury, and other inflammatory conditions induces neural activation in the celiac ganglion (3), followed by the production of norepinephrine (NE) from the splenic nerves (4). NE (5) stimulates the release of acetylcholine from a novel CD4⁺ T cell subset that expresses choline acetyltransferase and β1/2 adrenergic receptor (AR) (6). Released acetylcholine (6) acts on macrophages expressing α7 nicotinic acetylcholine receptor (α7nAChR) to inhibit the expression of pro-inflammatory cytokines including TNFα. It is suggested that C1 neurons in the medullary reticular formation of the brain mediate the anti-inflammatory effect.