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. 2019 Apr 2;16:69. doi: 10.1186/s12974-019-1455-y

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 9 — Working model of TGFβ1 signaling during AOM-induced HE. AOM-induced liver failure leads to an increase of hepatic TGFβ1 that enters the bloodstream, crosses the blood–brain barrier, and enters the brain. This results in the activation of TGFβR2 on neurons leading to increased expression and secretion of CCL2 and decreased expression and secretion of CX3CL1 from neurons. This imbalance of CCL2 and CX3CL1 leads to changes in chemokine receptor-mediated signaling in microglia, which ultimately results in microglia activation and worse HE outcomes