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. 2022 Jun 14;13:913178. doi: 10.3389/fimmu.2022.913178

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Copyright © 2022 Wang, Li, Liu, Luo, Guo, Yang, Xu, Ma and Chen

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 mechanisms of intestinal barrier disruption mediated by intestinal bacterial dysbiosis. The increase of intestinal pathogenic bacteria and the decrease of commensal metabolites in severe acute pancreatitis (SAP) jointly lead to the thinning of the intestinal mucus layer and the decrease of antimicrobial peptides (AMPs), mucin2 (MUC2), and IgA (SIgA) secretion, resulting in direct contact of pathogenic bacteria with the intestinal epithelial cells (IECs) and an “inflammatory storm”. The abnormal immune responses further lead to IEC damage, slow renewal, and disruption of the tight junctions (TJs) in epithelial cells, further stimulating excessive pro-inflammatory factors on the intestinal mucosal immune system. Finally, the integrity of the intestinal barrier is destroyed, bacteria and products translocate to the lungs, and then PALI ensues.