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. 2022 Dec 16;13:1065608. doi: 10.3389/fmicb.2022.1065608

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Copyright © 2022 Liang, Wu, Wang, Sun, Chen, Hu, Liu and Xing.

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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Bacteria species and functional pathways that are potentially promotive of IBD. Recent research identified many new bacteria species and the virulence factors they contain that potentially promote IBD. These virulence factors can directly bind to receptors on IECs and damage barrier function. Specific miRNAs are involved in regulating signaling pathways that further regulate immune cells to alter normal inflammatory responses. Moreover, bacteria-expressed sulfate esterases catalyze mucin O-glycans, which leads to mucin degradation, and ultimately worsens IBD. Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6), Bacteroides fragilis toxin (BFT), PHD finger protein 5A (PHF5A), Histone acetyltransferase KAT2A, Type 5 secretion systems (T5SS), FadA adhesion gene, Pore-forming toxins (Epxs), Human leukocyte antigen class I (HLA-I), Peripheral blood mononuclear cells (PBMCs), Intramolecular trans-sialidase (RgNanH), Sulfate esterase (BT1636^3S-Gal), tight junction proteins (ZO-1 and occludin), Cardiac glycoside reductase (cgr2).