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. 2021 Feb 8;27(1):141–153. doi: 10.1038/s41380-021-01032-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Gut dysbiosis (i.e., reduced gut-microbial diversity) has been shown to trigger: a a local inflammatory response (alpha-1-antitrypsin; I-FABP); b loosening of tight-junction proteins (zonulin); c translocation of bacterial endotoxin from the gut lumen to the bloodstream (LPS, ASCA, etc.); d activation of a systemic low-grade inflammation (LBP, sCD14, antibodies against bacterial endotoxin). Experimental models of gut dysbiosis showed a causative link with symptoms of sickness behavior (more details in main text).