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. 2022 Jul 22;9:961703. doi: 10.3389/fmed.2022.961703

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Copyright © 2022 Zheng, Tang, Hu and Zhang.

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) and the copyright owner(s) 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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Tryptophan metabolism controlled by gut microbiota regulates gastrointestinal (GI) motility. Tryptophan can be metabolized by gut microbiota to a variety of active substances. Aryl hydrocarbon receptor (AhR) ligands binding to AhR expressed on enteric neurons promote GI motility. Tryptamine contributes to fluid secretion by activating the 5-hydroxytryptamine (5-HT) receptor on enterocytes, which increases GI motility. Indole derivatives stimulate the release of 5-HT from enterochromaffin (EC) cells via transient receptor potential ankyrin A1 (Trpa1), which improves GI motility through stimulating intrinsic afferent primary neurons (IPANs). 5-hydroxyindole (5-HI) can directly act on smooth muscle cells via L-type voltage-dependent calcium channels (L-VDCCs) and then promotes GI motility.