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. 2021 Jul 27;13(1):1949096. doi: 10.1080/19490976.2021.1949096

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© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Intestinal fibrosis development during microbiota dysbiosis in Crohn’s disease. Mediators generated during sustained inflammation and continued PBT favored by gut barrier distortion induce myofibroblasts activation and extracellular matrix production with deposition of fibrinogen and collagen. Intestinal epithelial cells undergo EMT after activation of TLR-4 and contribute to the fibrotic context by inducing TGF-β. PBT, pathological bacterial translocation; TLRs, Toll-like receptors; ECM, extracellular matrix; EMT, epithelial to mesenchymal transition; ROs, reactive oxygen species; RNs, reactive nitrogen species; MCP-1, Monocyte Chemoattractant Protein-1; IL, interleukin; TGF-β, transforming growth factor-beta; SPF, Specific-pathogen-free; EIEC, Enteroinvasive Escherichia coli.