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. 2020 Jun;62:68–75. doi: 10.1016/j.conb.2019.11.020

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© 2019 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Neuron-macrophage crosstalk in the gut.

During homeostasis, enteric neurons maintain the muscularis macrophage (mMφ) population through the production of colony stimulating factor-1 (CSF-1), a growth factor necessary for Mφ survival. Reciprocally, mMφ directly control neuronal survival via the release of bone morphogenic protein type 2 (BMP2). During inflammation, cholinergic enteric neurons dampen mMφ activation via the interaction of acetylcholine (ACh) and α7 nicotinic acetylcholine receptor (α7 nAChR). In addition, in the context of bacterial infection extrinsic sympathetic fibers release noradrenaline (NE) promoting a tissue-protective phenotype in mMφ expressing β2 adrenergic receptor (β2-AR). Other abbreviations: CSF-1R, colony stimulating factor-1 receptor; BMP2R, bone morphogenic protein type 2 receptor.