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. 2022 Jan 25;15:781215. doi: 10.3389/fnins.2021.781215

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Copyright © 2022 Yang, Tan, Lin, Su, Li, Qi, Wang, Yang and Liu.

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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The mechanism of low-grade inflammation in gastroduodenal tissue. Th2 cell was activated in the duodenum, possibly by bacterium or antigens, which crossed the epithelium after impairing of mucosal integrity. Activated eosinophil acted as antigen-presenting cell to Th2-lymphocytes with Ig class switching of B cells to proallergic IgE-antibodies via IL-4 or IL-13. Besides, Th2 cell was the key driver of mast cell and eosinophil via IL-4/13 or IL-5, separately. Activated eosinophil released major basic protein (MBP), eosinophil derived neurotoxin (EDN) and others, which regulated the plasticity of peripheral nerve and then caused visceral hypersensitivity. Gut-homing T cells and other immune cells (expressing α4β7 and CCR9) may also increase in number and produce excess inflammatory cytokines that could increase vascular permeability and alter smooth muscle contraction and then delay gastric empty.